Volume 12, Issue 11

In silico phenotype projection of endothelial ERK1/2 signaling

Michael Simons, Jeffrey R. Gulcher, Thomas W. Chittenden,

https://doi.org/10.18632/aging.103529 pp 10001—10003

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Simons M, Gulcher JR, Chittenden TW, . In silico phenotype projection of endothelial ERK1/2 signaling. . 12:10001-10003. https://doi.org/10.18632/aging.103529

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COVID-19
From causes of aging to death from COVID-19

Mikhail V. Blagosklonny,

https://doi.org/10.18632/aging.103493 pp 10004—10021

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Blagosklonny MV, . From causes of aging to death from COVID-19. . 12:10004-10021. https://doi.org/10.18632/aging.103493

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                TY  - JOUR
                AU  - Blagosklonny, Mikhail V. 
                TI  - From causes of aging to death from COVID-19
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103493
                DO  - 10.18632/aging.103493
                SP  - 10004
                EP  - 10021
                PY  - 
                AB  - COVID-19 is not deadly early in life, but mortality increases exponentially with age, which is the strongest predictor of mortality. Mortality is higher in men than in women, because men age faster, and it is especially high in patients with age-related diseases, such as diabetes and hypertension, because these diseases are manifestations of aging and a measure of biological age. At its deepest level, aging (a program-like continuation of developmental growth) is driven by inappropriately high cellular functioning. The hyperfunction theory of quasi-programmed aging explains why COVID-19 vulnerability (lethality) is an age-dependent syndrome, linking it to other age-related diseases. It also explains inflammaging and immunosenescence, hyperinflammation, hyperthrombosis, and cytokine storms, all of which are associated with COVID-19 vulnerability. Anti-aging interventions, such as rapamycin, may slow aging and age-related diseases, potentially decreasing COVID-19 vulnerability.
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COVID-19
Potential mechanisms of hemorrhagic stroke in elderly COVID-19 patients

Haili Wang, Xiaojia Tang, Hongyang Fan, Yuhan Luo, Yuxia Song, Yao Xu, Yingzhu Chen,

https://doi.org/10.18632/aging.103335 pp 10022—10034

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Wang H, Tang X, Fan H, Luo Y, Song Y, Xu Y, Chen Y, . Potential mechanisms of hemorrhagic stroke in elderly COVID-19 patients. . 12:10022-10034. https://doi.org/10.18632/aging.103335

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                TY  - JOUR
                AU  - Wang, Haili 
                AU  - Tang, Xiaojia 
                AU  - Fan, Hongyang 
                AU  - Luo, Yuhan 
                AU  - Song, Yuxia 
                AU  - Xu, Yao 
                AU  - Chen, Yingzhu 
                TI  - Potential mechanisms of hemorrhagic stroke in elderly COVID-19 patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103335
                DO  - 10.18632/aging.103335
                SP  - 10022
                EP  - 10034
                PY  - 
                AB  - The novel severe acute respiratory syndrome coronavirus 2 is the causative agent of coronavirus disease 2019, a new human infectious disease. While fever, cough, and respiratory distress are typical first symptoms, a fraction of those affected present instead with neurological symptoms suggestive of central nervous system compromise. This review summarizes the potential contribution of coronavirus disease 2019 to hemorrhagic stroke in the elderly and proposes possible mechanisms. Reports show that the most affected patients have underlying chronic diseases such as hypertension and diabetes, which are two key risk factors for hemorrhagic stroke. Angiotensin-converting enzyme 2 is the main host cell surface receptor interacting with the severe acute respiratory syndrome coronavirus 2 spike glycoprotein to allow viral entry and infection. We speculate that ensuing downregulation of angiotensin-converting enzyme 2 expression may compound the risk conferred by pre-existing comorbidities and critically influence the pathogenesis of hemorrhagic stroke by elevating blood pressure and impairing cerebrovascular endothelial function. Additionally, both age- and/or disease-related immune dysfunction and enhanced catecholamine release secondary to anxiety and stress may also aggravate central nervous system symptoms of severe acute respiratory syndrome coronavirus 2 infection. Thus, assessment of systemic inflammatory biomarkers and tight control of hemodynamic parameters upon admission are crucial to minimize mortality and morbidity in coronavirus disease 2019 patients with central nervous system symptoms suggestive of incipient stroke.
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COVID-19
Microdose lithium reduces cellular senescence in human astrocytes - a potential pharmacotherapy for COVID-19?

Tania Viel, Shankar Chinta, Anand Rane, Manish Chamoli, Hudson Buck, Julie Andersen,

https://doi.org/10.18632/aging.103449 pp 10035—10040

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Viel T, Chinta S, Rane A, Chamoli M, Buck H, Andersen J, . Microdose lithium reduces cellular senescence in human astrocytes - a potential pharmacotherapy for COVID-19?. . 12:10035-10040. https://doi.org/10.18632/aging.103449

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                TY  - JOUR
                AU  - Viel, Tania 
                AU  - Chinta, Shankar 
                AU  - Rane, Anand 
                AU  - Chamoli, Manish 
                AU  - Buck, Hudson 
                AU  - Andersen, Julie 
                TI  - Microdose lithium reduces cellular senescence in human astrocytes - a potential pharmacotherapy for COVID-19?
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103449
                DO  - 10.18632/aging.103449
                SP  - 10035
                EP  - 10040
                PY  - 
                AB  - Cell senescence is a process that causes growth arrest and the release of a senescence associated secretory phenotype (SASP), characterized by secretion of chemokines, cytokines, cell growth factors and metalloproteases, leading to a tissue condition that may precipitate cancers and neurodegenerative processes. With the recent pandemic of coronavirus, senolytic drugs are being considered as possible therapeutic tools to reduce the virulence of SARS-CoV-2. In the last few years, our research group showed that lithium carbonate at microdose levels was able to stabilize memory and change neuropathological characteristics of Alzheimer&#x2019;s disease (AD). In the present work, we present evidence that low-dose lithium can reduce the SASP of human iPSCs-derived astrocytes following acute treatment, suggesting that microdose lithium could protect cells from senescence and development of aging-related conditions. With the present findings, a perspective of the potential use of low-dose lithium in old patients from the &#x201C;high risk group&#x201D; for COVID-19 (with hypertension, diabetes and chronic obstructive pulmonary disease) is presented.
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Lactate dehydrogenase expression modulates longevity and neurodegeneration in Drosophila melanogaster

Dani M. Long, Ariel K. Frame, Patrick N. Reardon, Robert C. Cumming, David A. Hendrix, Doris Kretzschmar, Jadwiga M. Giebultowicz,

https://doi.org/10.18632/aging.103373 pp 10041—10058

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Long DM, Frame AK, Reardon PN, Cumming RC, Hendrix DA, Kretzschmar D, Giebultowicz JM, . Lactate dehydrogenase expression modulates longevity and neurodegeneration in Drosophila melanogaster. . 12:10041-10058. https://doi.org/10.18632/aging.103373

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Provider: 
 TY - JOUR
 AU - Long, Dani M. 
 AU - Frame, Ariel K. 
 AU - Reardon, Patrick N. 
 AU - Cumming, Robert C. 
 AU - Hendrix, David A. 
 AU - Kretzschmar, Doris 
 AU - Giebultowicz, Jadwiga M. 
 TI - Lactate dehydrogenase expression modulates longevity and neurodegeneration in Drosophila melanogaster
 JO - 
 JA - 
 VL - 12
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103373
 DO - 10.18632/aging.103373
 SP - 10041
 EP - 10058
 PY - 
 AB - Lactate dehydrogenase (LDH) catalyzes the conversion of glycolysis-derived pyruvate to lactate. Lactate has been shown to play key roles in brain energetics and memory formation. However, lactate levels are elevated in aging and Alzheimer&#x2019;s disease patients, and it is not clear whether lactate plays protective or detrimental roles in these contexts. Here we show that Ldh transcript levels are elevated and cycle with diurnal rhythm in the heads of aged flies and this is associated with increased LDH protein, enzyme activity, and lactate concentrations. To understand the biological significance of increased Ldh gene expression, we genetically manipulated Ldh levels in adult neurons or glia. Overexpression of Ldh in both cell types caused a significant reduction in lifespan whereas Ldh down-regulation resulted in lifespan extension. Moreover, pan-neuronal overexpression of Ldh disrupted circadian locomotor activity rhythms and significantly increased brain neurodegeneration. In contrast, reduction of Ldh in neurons delayed age-dependent neurodegeneration. Thus, our unbiased genetic approach identified Ldh and lactate as potential modulators of aging and longevity in flies.
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COVID-19
Infection with SARS-CoV-2 causes abnormal laboratory results of multiple organs in patients

Ai-Ping Yang, Hui-Ming Li, Wen-Qiang Tao, Xue-Jing Yang, Min Wang, Wen-Juan Yang, Jian-Ping Liu,

https://doi.org/10.18632/aging.103255 pp 10059—10069

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Yang A, Li H, Tao W, Yang X, Wang M, Yang W, Liu J, . Infection with SARS-CoV-2 causes abnormal laboratory results of multiple organs in patients. . 12:10059-10069. https://doi.org/10.18632/aging.103255

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                TY  - JOUR
                AU  - Yang, Ai-Ping 
                AU  - Li, Hui-Ming 
                AU  - Tao, Wen-Qiang 
                AU  - Yang, Xue-Jing 
                AU  - Wang, Min 
                AU  - Yang, Wen-Juan 
                AU  - Liu, Jian-Ping 
                TI  - Infection with SARS-CoV-2 causes abnormal laboratory results of multiple organs in patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103255
                DO  - 10.18632/aging.103255
                SP  - 10059
                EP  - 10069
                PY  - 
                AB  - Aim: To evaluate the clinical value of abnormal laboratory results of multiple organs in patients with coronavirus disease 2019 (COVID-2019) and to help clinicians perform correct treatment.Results: Elevated neutrophil-to-LYM ratio (NLR), D-dimer(D-D), interleukin (IL)-6, IL-10, IL-2, interferon-Y, and age were significantly associated with the severity of illness. However, significant and sustained decreases were observed in the LYM subset (p&lt;0.05). D-D, T cell counts, and cytokine levels in severe COVID-19 patients who survived the disease gradually recovered at later time points to levels that were comparable to those of mild cases. Second, D-D increased from 0.5 to 8, and the risk ratio increased from 2.75 to 55, eventually leading to disseminated intravascular coagulation. Moreover, the acute renal function damage occurred earlier than abnormal heart and liver functions (p&lt;0.05).Conclusions: The degrees of lymphopenia and proinflammatory cytokine storm were higher in severe COVID-19 patients than in mild cases. The degree was associated with the disease severity. Advanced age, NLR, D-D, and cytokine levels may serve as useful prognostic factors for the early identification of severe COVID-19 cases.Methods: Peripheral blood samples were collected from 93 confirmed COVID-19 patients. The samples were examined for lymphocyte (LYM) subsets by flow cytometry and cytokine profiles by specific immunoassays. The receiver operating characteristic curve was applied to determine the best diagnostic thresholds for laboratory results, and principal component analysis was used to screen the major risk factors. The prognostic values were assessed using the Kaplan&#x2013;Meier curve and univariate and multivariate COX regression models.
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COVID-19
Comparison of clinical characteristics and outcomes of patients with coronavirus disease 2019 at different ages

Mengmeng Zhao, Menglong Wang, Jishou Zhang, Jian Gu, Pingan Zhang, Yao Xu, Jing Ye, Zhen Wang, Di Ye, Wei Pan, Bo Shen, Hua He, Mingxiao Liu, Menglin Liu, Zhen Luo, Dan Li, Jianfang Liu, Jun Wan,

https://doi.org/10.18632/aging.103298 pp 10070—10086

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Zhao M, Wang M, Zhang J, Gu J, Zhang P, Xu Y, Ye J, Wang Z, Ye D, Pan W, Shen B, He H, Liu M, et al, . Comparison of clinical characteristics and outcomes of patients with coronavirus disease 2019 at different ages. . 12:10070-10086. https://doi.org/10.18632/aging.103298

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                TY  - JOUR
                AU  - Zhao, Mengmeng 
                AU  - Wang, Menglong 
                AU  - Zhang, Jishou 
                AU  - Gu, Jian 
                AU  - Zhang, Pingan 
                AU  - Xu, Yao 
                AU  - Ye, Jing 
                AU  - Wang, Zhen 
                AU  - Ye, Di 
                AU  - Pan, Wei 
                AU  - Shen, Bo 
                AU  - He, Hua 
                AU  - Liu, Mingxiao 
                AU  - Liu, Menglin 
                AU  - Luo, Zhen 
                AU  - Li, Dan 
                AU  - Liu, Jianfang 
                AU  - Wan, Jun 
                TI  - Comparison of clinical characteristics and outcomes of patients with coronavirus disease 2019 at different ages
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103298
                DO  - 10.18632/aging.103298
                SP  - 10070
                EP  - 10086
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Zhao, Mengmeng 
                AU  - Wang, Menglong 
                AU  - Zhang, Jishou 
                AU  - Gu, Jian 
                AU  - Zhang, Pingan 
                AU  - Xu, Yao 
                AU  - Ye, Jing 
                AU  - Wang, Zhen 
                AU  - Ye, Di 
                AU  - Pan, Wei 
                AU  - Shen, Bo 
                AU  - He, Hua 
                AU  - Liu, Mingxiao 
                AU  - Liu, Menglin 
                AU  - Luo, Zhen 
                AU  - Li, Dan 
                AU  - Liu, Jianfang 
                AU  - Wan, Jun 
                TI  - Comparison of clinical characteristics and outcomes of patients with coronavirus disease 2019 at different ages
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103298
                DO  - 10.18632/aging.103298
                SP  - 10070
                EP  - 10086
                PY  - 
                AB  - Background: Information about the clinical characteristics and mortality of patients with coronavirus disease 2019 at different ages is limited.Results: The older group had more patients with dyspnea and fewer patients with fever and muscle pain. Older patients had more underlying diseases, secondary infection, myocardial injury, renal dysfunction, coagulation dysfunction, and immune dysfunction on admission. More older patients received immunoglobulin therapy and mechanical ventilation. The proportions of patients with multiple organ injuries, critically ill patients and death increased significantly with age. The older groups had higher cumulative death risk than the younger group. Hypertension, cerebrovascular disease, comorbidities, acute cardiac injury, shock and complications are independent predictors of death.Conclusions: The symptoms of the elderly patients were more atypical, with more comorbidities, secondary infection, organ injuries, immune dysfunction and a higher risk of critical illness. Older age was an important risk factor for mortality.Methods: 1000 patients diagnosed with coronavirus disease 2019 from January 1, 2020 to February 14, 2020 were enrolled. According to age, patients were divided into group 1 (&lt;60 years old), group 2 (60-74 years old) and group 3 (&#x2265;75 years old). The clinical symptoms, first laboratory results, CT findings, organ injuries, disease severity and mortality were analyzed.
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COVID-19
ACE2 and TMPRSS2 variants and expression as candidates to sex and country differences in COVID-19 severity in Italy

Rosanna Asselta, Elvezia Maria Paraboschi, Alberto Mantovani, Stefano Duga,

https://doi.org/10.18632/aging.103415 pp 10087—10098

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Asselta R, Paraboschi EM, Mantovani A, Duga S, . ACE2 and TMPRSS2 variants and expression as candidates to sex and country differences in COVID-19 severity in Italy. . 12:10087-10098. https://doi.org/10.18632/aging.103415

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 TY - JOUR
 AU - Asselta, Rosanna 
 AU - Paraboschi, Elvezia Maria 
 AU - Mantovani, Alberto 
 AU - Duga, Stefano 
 TI - ACE2 and TMPRSS2 variants and expression as candidates to sex and country differences in COVID-19 severity in Italy
 JO - 
 JA - 
 VL - 12
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103415
 DO - 10.18632/aging.103415
 SP - 10087
 EP - 10098
 PY - 
 AB - As the outbreak of coronavirus disease 2019 (COVID-19) progresses, prognostic markers for early identification of high-risk individuals are an urgent medical need. Italy has one of the highest numbers of SARS-CoV-2-related deaths and one of the highest mortality rates. Worldwide, a more severe course of COVID-19 is associated with older age, comorbidities, and male sex. Hence, we searched for possible genetic components of COVID-19 severity among Italians by looking at expression levels and variants in ACE2 and TMPRSS2 genes, crucial for viral infection.Exome and SNP-array data from a large Italian cohort were used to compare the rare-variants burden and polymorphisms frequency with Europeans and East Asians. Moreover, we looked into gene expression databases to check for sex-unbalanced expression.While we found no significant evidence that ACE2 is associated with disease severity/sex bias, TMPRSS2 levels and genetic variants proved to be possible candidate disease modulators, prompting for rapid experimental validations on large patient cohorts.
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Age-related cognitive decline in baboons: modeling the prodromal phase of Alzheimer's disease and related dementias

Stephanny Lizarraga, Etienne W. Daadi, Gourav Roy-Choudhury, Marcel M. Daadi,

https://doi.org/10.18632/aging.103272 pp 10099—10116

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Lizarraga S, Daadi EW, Roy-Choudhury G, Daadi MM, . Age-related cognitive decline in baboons: modeling the prodromal phase of Alzheimer's disease and related dementias. . 12:10099-10116. https://doi.org/10.18632/aging.103272

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                TY  - JOUR
                AU  - Lizarraga, Stephanny 
                AU  - Daadi, Etienne W. 
                AU  - Roy-Choudhury, Gourav 
                AU  - Daadi, Marcel M. 
                TI  - Age-related cognitive decline in baboons: modeling the prodromal phase of Alzheimer's disease and related dementias
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103272
                DO  - 10.18632/aging.103272
                SP  - 10099
                EP  - 10116
                PY  - 
                AB  - The aging of brain cells and synaptic loss are the major underlying pathophysiological processes contributing to the progressive decline in cognitive functions and Alzheimer&#x2019;s disease. The difference in cognitive performances observed between adult and aged subjects across species highlights the decline of brain systems with age. The inflection point in age-related cognitive decline is important for our understanding of the pathophysiology of neurodegenerative diseases and for timing therapeutic interventions. Humans and nonhuman primates share many similarities including age-dependent changes in gene expression and decline in neural and immune functions. Given these evolutionary conserved organ systems, complex human-like behavioral and age-dependent changes may be modeled and monitored longitudinally in nonhuman primates. We integrated three clinically relevant outcome measures to investigate the effect of age on cognition, motor function and diurnal activity in aged baboons. We provide evidence of a naturally-occurring age-dependent precipitous decline in movement planning, in learning novel tasks, in simple discrimination and in motivation. These results suggest that baboons aged ~20 years (equivalent to ~60 year old humans) may offer a relevant model for the prodromal phase of Alzheimer&#x2019;s disease and related dementias to investigate mechanisms involved in the precipitous decline in cognitive functions and to develop early therapeutic interventions
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Salvianolic Acid B improves cognitive impairment by inhibiting neuroinflammation and decreasing Aβ level in Porphyromonas gingivalis-infected mice

Jianwei Liu, Yiling Wang, Jing Guo, Jinyan Sun, Qinfeng Sun,

https://doi.org/10.18632/aging.103306 pp 10117—10128

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Liu J, Wang Y, Guo J, Sun J, Sun Q, . Salvianolic Acid B improves cognitive impairment by inhibiting neuroinflammation and decreasing Aβ level in Porphyromonas gingivalis-infected mice. . 12:10117-10128. https://doi.org/10.18632/aging.103306

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Provider: 
 TY - JOUR
 AU - Liu, Jianwei 
 AU - Wang, Yiling 
 AU - Guo, Jing 
 AU - Sun, Jinyan 
 AU - Sun, Qinfeng 
 TI - Salvianolic Acid B improves cognitive impairment by inhibiting neuroinflammation and decreasing Aβ level in Porphyromonas gingivalis-infected mice
 JO - 
 JA - 
 VL - 12
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103306
 DO - 10.18632/aging.103306
 SP - 10117
 EP - 10128
 PY - 
 AB - Amyloid-&#x3B2; (A&#x3B2;) accumulation is one of the main pathological hallmarks of Alzheimer&#x2019;s disease (AD). Porphyromonas gingivalis (P. gingivalis), the pathogen of chronic periodontitis, could cause A&#x3B2; accumulation and was identified in the brain of AD patients. Salvianolic Acid B (SalB) has been proven to have the neuroprotective effect. Whether SalB could protect against P. gingivalis-induced cognitive impairment is still unknown. In this study, a P. gingivalis-infected mouse model was employed to study the neuroprotective role of SalB. The results showed that SalB (20 and 40 mg/kg) treatment for 4 weeks could shorten the escape latency and improve the percentage of spontaneous alternation in the P. gingivalis-infected mice. SalB inhibited the levels of reactive oxygen species and malondialdehyde, while increased the levels of antioxidative enzymes (superoxide dismutase and glutathione peroxidase). SalB decreased the levels of IL-1&#x3B2; and IL-6, increased the mRNA levels of bdnf and ngf in the brain of P. gingivalis-infected mice. In addition, SalB obviously decreased the level of A&#x3B2;. SalB elevated the protein expression of ADAM10, while downregulated BACE1 and PS1. SalB increased the protein expression of LRP1, while decreased RAGE. In conclusion, SalB could improve cognitive impairment by inhibiting neuroinflammation and decreasing A&#x3B2; level in P. gingivalis-infected mice.
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Clusterin exerts a cytoprotective and antioxidant effect in human osteoarthritic cartilage

Chiara Tarquini, Sabina Pucci, Maria Giovanna Scioli, Elena Doldo, Sara Agostinelli, Federico D’Amico, Alessandra Bielli, Amedeo Ferlosio, Emanuele Caredda, Umberto Tarantino, Augusto Orlandi,

https://doi.org/10.18632/aging.103310 pp 10129—10146

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Tarquini C, Pucci S, Scioli MG, Doldo E, Agostinelli S, D’Amico F, Bielli A, Ferlosio A, Caredda E, Tarantino U, Orlandi A, . Clusterin exerts a cytoprotective and antioxidant effect in human osteoarthritic cartilage. . 12:10129-10146. https://doi.org/10.18632/aging.103310

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                TY  - JOUR
                AU  - Tarquini, Chiara 
                AU  - Pucci, Sabina 
                AU  - Scioli, Maria Giovanna 
                AU  - Doldo, Elena 
                AU  - Agostinelli, Sara 
                AU  - D’Amico, Federico 
                AU  - Bielli, Alessandra 
                AU  - Ferlosio, Amedeo 
                AU  - Caredda, Emanuele 
                AU  - Tarantino, Umberto 
                AU  - Orlandi, Augusto 
                TI  - Clusterin exerts a cytoprotective and antioxidant effect in human osteoarthritic cartilage
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103310
                DO  - 10.18632/aging.103310
                SP  - 10129
                EP  - 10146
                PY  - 
                AB  - Osteoarthritis (OA) is the most common joint disease characterized by destruction of articular cartilage. OA-induced cartilage degeneration causes inflammation, oxidative stress and the hypertrophic shift of quiescent chondrocytes. Clusterin (CLU) is a ubiquitous glycoprotein implicated in many cellular processes and its upregulation has been recently reported in OA cartilage. However, the specific role of CLU in OA cartilage injury has not been investigated yet. We analyzed CLU expression in human articular cartilage in vivo and in cartilage-derived chondrocytes in vitro. CLU knockdown in OA chondrocytes was also performed and its effect on proliferation, hypertrophic phenotype, apoptosis, inflammation and oxidative stress was investigated. CLU expression was upregulated in human OA cartilage and in cultured OA cartilage-derived chondrocytes compared with control group. CLU knockdown reduced cell proliferation and increased hypertrophic phenotype as well as apoptotic death. CLU-silenced OA chondrocytes showed higher MMP13 and COL10A1 as well as greater TNF-&#x3B1;, Nox4 and ROS levels. Our results indicate a possible cytoprotective role of CLU in OA chondrocytes promoting cell survival by its anti-apoptotic, anti-inflammatory and antioxidant properties and counteracting the hypertrophic phenotypic shift. Further studies are needed to deepen the role of CLU in order to identify a new potential therapeutic target for OA.
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Chronic polypharmacy impairs explorative behavior and reduces synaptic functions in young adult mice

Francesca Eroli, Kristina Johnell, María Latorre Leal, Chiara Adamo, Sarah Hilmer, Jonas W. Wastesson, Angel Cedazo-Minguez, Silvia Maioli,

https://doi.org/10.18632/aging.103315 pp 10147—10161

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Eroli F, Johnell K, Latorre Leal M, Adamo C, Hilmer S, Wastesson JW, Cedazo-Minguez A, Maioli S, . Chronic polypharmacy impairs explorative behavior and reduces synaptic functions in young adult mice. . 12:10147-10161. https://doi.org/10.18632/aging.103315

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                TY  - JOUR
                AU  - Eroli, Francesca 
                AU  - Johnell, Kristina 
                AU  - Latorre Leal, María 
                AU  - Adamo, Chiara 
                AU  - Hilmer, Sarah 
                AU  - Wastesson, Jonas W. 
                AU  - Cedazo-Minguez, Angel 
                AU  - Maioli, Silvia 
                TI  - Chronic polypharmacy impairs explorative behavior and reduces synaptic functions in young adult mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103315
                DO  - 10.18632/aging.103315
                SP  - 10147
                EP  - 10161
                PY  - 
                AB  - A major challenge in the health care system is the lack of knowledge about the possible harmful effects of multiple drug treatments in old age. The present study aims to characterize a mouse model of polypharmacy, in order to investigate whether long-term exposure to multiple drugs could lead to adverse outcomes. To this purpose we selected five drugs from the ten most commonly used by older adults in Sweden (metoprolol, paracetamol, aspirin, simvastatin and citalopram). Five-month-old wild type male mice were fed for eight weeks with control or polypharmacy diet. We report for the first time that young adult polypharmacy-treated mice showed a significant decrease in exploration and spatial working memory compared to the control group. This memory impairment was further supported by a significant reduction of synaptic proteins in the hippocampus of treated mice. These novel results suggest that already at young adult age, use of polypharmacy affects explorative behavior and synaptic functions. This study underlines the importance of investigating the potentially negative outcomes from concomitant administration of different drugs, which have been poorly explored until now. The mouse model proposed here has translatable findings and can be applied as a useful tool for future studies on polypharmacy.
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First-in-class candidate therapeutics that target mitochondria and effectively prevent cancer cell metastasis: mitoriboscins and TPP compounds

Béla Ózsvári, Federica Sotgia, Michael P. Lisanti,

https://doi.org/10.18632/aging.103336 pp 10162—10179

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Ózsvári B, Sotgia F, Lisanti MP, . First-in-class candidate therapeutics that target mitochondria and effectively prevent cancer cell metastasis: mitoriboscins and TPP compounds. . 12:10162-10179. https://doi.org/10.18632/aging.103336

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                TY  - JOUR
                AU  - Ózsvári, Béla 
                AU  - Sotgia, Federica 
                AU  - Lisanti, Michael P. 
                TI  - First-in-class candidate therapeutics that target mitochondria and effectively prevent cancer cell metastasis: mitoriboscins and TPP compounds
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103336
                DO  - 10.18632/aging.103336
                SP  - 10162
                EP  - 10179
                PY  - 
                AB  - Cancer stem cells (CSCs) have been proposed to be responsible for tumor recurrence, distant metastasis and drug-resistance, in the vast majority of cancer patients. Therefore, there is an urgent need to identify new drugs that can target and eradicate CSCs. To identify new molecular targets that are unique to CSCs, we previously compared MCF7 2D-monolayers with 3D-mammospheres, which are enriched in CSCs. We observed that 25 mitochondrial-related proteins were &gt;100-fold over-expressed in 3D-mammospheres. Here, we used these 25 proteins to derive short gene signatures to predict distant metastasis (in N=1,395 patients) and tumor recurrence (in N=3,082 patients), by employing a large collection of transcriptional profiling data from ER(+) breast cancer patients. This analysis resulted in a 4-gene signature for predicting distant metastasis, with a hazard ratio of 1.91-fold (P=2.2e-08). This provides clinical evidence to support a role for CSC mitochondria in metastatic dissemination. Next, we employed a panel of mitochondrial inhibitors, previously shown to target mitochondria and selectively inhibit 3D-mammosphere formation in MCF7 cells and cell migration in MDA-MB-231 cells. Remarkably, these five mitochondrial inhibitors had only minor effects or no effect on MDA-MB-231 tumor formation, but preferentially and selectively inhibited tumor cell metastasis, without causing significant toxicity. Mechanistically, all five mitochondrial inhibitors have been previously shown to induce ATP-depletion in cancer cells. Since 3 of these 5 inhibitors were designed to target the large mitochondrial ribosome, we next interrogated whether genes encoding the large mitochondrial ribosomal proteins (MRPL) also show prognostic value in the prediction of distant metastasis in both ER(+) and ER(-) breast cancer patients. Interestingly, gene signatures composed of 6 to 9 MRPL mRNA-transcripts were indeed sufficient to predict distant metastasis, tumor recurrence and Tamoxifen resistance. These gene signatures could be useful as companion diagnostics to assess which patients may benefit most from anti-mito-ribosome therapy. Overall, our studies provide the necessary proof-of-concept, and in vivo functional evidence, that mitochondrial inhibitors can successfully and selectively target the biological process of cancer cell metastasis. Ultimately, we envision that mitochondrial inhibitors could be employed to develop new treatment protocols, for clinically providing metastasis prophylaxis, to help prevent poor clinical outcomes in cancer patients.
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Reduced expression of microRNA-130a promotes endothelial cell senescence and age-dependent impairment of neovascularization

Wahiba Dhahri, Sylvie Dussault, Éliane Légaré, François Rivard, Michel Desjarlais, Raphael Mathieu, Alain Rivard,

https://doi.org/10.18632/aging.103340 pp 10180—10193

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Dhahri W, Dussault S, Légaré É, Rivard F, Desjarlais M, Mathieu R, Rivard A, . Reduced expression of microRNA-130a promotes endothelial cell senescence and age-dependent impairment of neovascularization. . 12:10180-10193. https://doi.org/10.18632/aging.103340

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                TY  - JOUR
                AU  - Dhahri, Wahiba 
                AU  - Dussault, Sylvie 
                AU  - Légaré, Éliane 
                AU  - Rivard, François 
                AU  - Desjarlais, Michel 
                AU  - Mathieu, Raphael 
                AU  - Rivard, Alain 
                TI  - Reduced expression of microRNA-130a promotes endothelial cell senescence and age-dependent impairment of neovascularization
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103340
                DO  - 10.18632/aging.103340
                SP  - 10180
                EP  - 10193
                PY  - 
                AB  - Aging is associated with impaired neovascularization in response to ischemia. MicroRNAs are small noncoding RNAs emerging as key regulators of physiological and pathological processes. Here we investigated the potential role of microRNAs in endothelial cell senescence and age-dependent impairment of neovascularization. Next generation sequencing and qRT-PCR analyses identified miR-130a as a pro-angiogenic microRNA which expression is significantly reduced in old mouse aortic endothelial cells (ECs). Transfection of young ECs with a miR-130a inhibitor leads to accelerated senescence and reduced angiogenic functions. Conversely, forced expression of miR-130a in old ECs reduces senescence and improves angiogenesis. In a mouse model of hindlimb ischemia, intramuscular injection of miR-130a mimic in older mice restores blood flow recovery and vascular densities in ischemic muscles, improves mobility and reduces tissue damage. miR-130a directly targets antiangiogenic homeobox genes MEOX2 and HOXA5. MEOX2 and HOXA5 are significantly increased in the ischemic muscles of aging mice, but forced expression of miR-130a reduces the expression of these factors. miR-130a treatment after ischemia is also associated with increased number and improved functional activities of pro-angiogenic cells (PACs). Forced expression of miR-130a could constitute a novel strategy to improve blood flow recovery and reduce ischemia in older patients with ischemic vascular diseases.
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Influences of TP53 and the anti-aging DDR1 receptor in controlling Raf/MEK/ERK and PI3K/Akt expression and chemotherapeutic drug sensitivity in prostate cancer cell lines

William H. Chappell, Saverio Candido, Stephen L. Abrams, Shaw M. Akula, Linda S. Steelman, Alberto M. Martelli, Stefano Ratti, Lucio Cocco, Melchiorre Cervello, Giuseppe Montalto, Ferdinando Nicoletti, Massimo Libra, James A. McCubrey,

https://doi.org/10.18632/aging.103377 pp 10194—10210

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Chappell WH, Candido S, Abrams SL, Akula SM, Steelman LS, Martelli AM, Ratti S, Cocco L, Cervello M, Montalto G, Nicoletti F, Libra M, McCubrey JA, . Influences of TP53 and the anti-aging DDR1 receptor in controlling Raf/MEK/ERK and PI3K/Akt expression and chemotherapeutic drug sensitivity in prostate cancer cell lines. . 12:10194-10210. https://doi.org/10.18632/aging.103377

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                TY  - JOUR
                AU  - Chappell, William H. 
                AU  - Candido, Saverio 
                AU  - Abrams, Stephen L. 
                AU  - Akula, Shaw M. 
                AU  - Steelman, Linda S. 
                AU  - Martelli, Alberto M. 
                AU  - Ratti, Stefano 
                AU  - Cocco, Lucio 
                AU  - Cervello, Melchiorre 
                AU  - Montalto, Giuseppe 
                AU  - Nicoletti, Ferdinando 
                AU  - Libra, Massimo 
                AU  - McCubrey, James A. 
                TI  - Influences of TP53 and the anti-aging DDR1 receptor in controlling Raf/MEK/ERK and PI3K/Akt expression and chemotherapeutic drug sensitivity in prostate cancer cell lines
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103377
                DO  - 10.18632/aging.103377
                SP  - 10194
                EP  - 10210
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Chappell, William H. 
                AU  - Candido, Saverio 
                AU  - Abrams, Stephen L. 
                AU  - Akula, Shaw M. 
                AU  - Steelman, Linda S. 
                AU  - Martelli, Alberto M. 
                AU  - Ratti, Stefano 
                AU  - Cocco, Lucio 
                AU  - Cervello, Melchiorre 
                AU  - Montalto, Giuseppe 
                AU  - Nicoletti, Ferdinando 
                AU  - Libra, Massimo 
                AU  - McCubrey, James A. 
                TI  - Influences of TP53 and the anti-aging DDR1 receptor in controlling Raf/MEK/ERK and PI3K/Akt expression and chemotherapeutic drug sensitivity in prostate cancer cell lines
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103377
                DO  - 10.18632/aging.103377
                SP  - 10194
                EP  - 10210
                PY  - 
                AB  - Background: TP53 plays critical roles in sensitivity to chemotherapy, and aging. Collagen is very important in aging. The molecular structure and biochemical properties of collagen changes during aging. The discoidin domain receptor (DDR1) is regulated in part by collagen. Elucidating the links between TP53 and DDR1 in chemosensitivity and aging could improve therapies against cancer and aging.Results: Restoration of WT-TP53 activity resulted in increased sensitivity to chemotherapeutic drugs and elevated expression of key components of the Raf/MEK/ERK, PI3K/Akt and DDR1 pathways. DDR1 could modulate the levels of Raf/MEK/ERK and PI3K/Akt pathways as well as sensitize the cells to chemotherapeutic drugs. In contrast, suppression of WT TP53 with a dominant negative (DN) TP53 gene, suppressed DDR1 protein levels and increased their chemoresistance.Conclusion: Restoration of WT TP53 activity or increased expression of the anti-aging DDR1 collagen receptor can result in enhanced sensitivity to chemotherapeutic drugs. Our innovative studies indicate the important links between WT TP53 and DDR1 which can modulate Raf/MEK/ERK and PI3K/Akt signaling as well as chemosensitivity and aging.Methods: We investigated the roles of wild type (WT) and mutant TP53 on drug sensitivity of prostate cancer cells and the induction of Raf/MEK/ERK, PI3K/Akt and DDR1 expression and chemosensitivity.
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Effects of intraovarian injection of autologous platelet rich plasma on ovarian reserve and IVF outcome parameters in women with primary ovarian insufficiency

Yigit Cakiroglu, Ayse Saltik, Aysen Yuceturk, Ozge Karaosmanoglu, Sule Yildirim Kopuk, Richard T. Scott Jr., Bulent Tiras, Emre Seli,

https://doi.org/10.18632/aging.103403 pp 10211—10222

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Cakiroglu Y, Saltik A, Yuceturk A, Karaosmanoglu O, Kopuk SY, Scott RT, Tiras B, Seli E, . Effects of intraovarian injection of autologous platelet rich plasma on ovarian reserve and IVF outcome parameters in women with primary ovarian insufficiency. . 12:10211-10222. https://doi.org/10.18632/aging.103403

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                TY  - JOUR
                AU  - Cakiroglu, Yigit 
                AU  - Saltik, Ayse 
                AU  - Yuceturk, Aysen 
                AU  - Karaosmanoglu, Ozge 
                AU  - Kopuk, Sule Yildirim 
                AU  - Scott, Richard T. 
                AU  - Tiras, Bulent 
                AU  - Seli, Emre 
                TI  - Effects of intraovarian injection of autologous platelet rich plasma on ovarian reserve and IVF outcome parameters in women with primary ovarian insufficiency
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103403
                DO  - 10.18632/aging.103403
                SP  - 10211
                EP  - 10222
                PY  - 
                AB  - We aimed to determine whether intraovarian injection of autologous platelet rich plasma (PRP) improves response to ovarian stimulation and in vitro fertilization (IVF) outcome in women with primary ovarian insufficiency (POI). Women (N=311; age 24-40) diagnosed with POI based on ESHRE criteria underwent intraovarian PRP injection. Markers of ovarian reserve, and IVF outcome parameters were followed. PRP treatment resulted in increased antral follicle count (AFC) and serum antimullerian hormone (AMH), while serum follicle stimulating hormone (FSH) did not change significantly. After PRP injection, 23 women (7.4%) conceived spontaneously, 201 (64.8%) developed antral follicle(s) and attempted IVF, and 87 (27.8%) had no antral follicles and therefore did not receive additional treatment. Among the 201 women who attempted IVF, 82 (26.4% of total) developed embryos; 25 of these women preferred to cryopreserve embryos for transfer at a later stage, while 57 underwent embryo transfer resulting in 13 pregnancies (22.8% per transfer, 4% of total). In total, of the 311 women treated with PRP, 25 (8.0%) achieved livebirth/sustained implantation (spontaneously or after IVF), while another 25 (8.0%) cryopreserved embryos. Our findings suggest that in women with POI, intraovarian injection of autologous PRP might be considered as an alternative experimental treatment option.
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Long non-coding RNA SNHG1 activates HOXA1 expression via sponging miR-193a-5p in breast cancer progression

Jun Li, Tianyu Zeng, Wei Li, Hao Wu, Chunxiao Sun, Fan Yang, Mengzhu Yang, Ziyi Fu, Yongmei Yin,

https://doi.org/10.18632/aging.103123 pp 10223—10234

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Li J, Zeng T, Li W, Wu H, Sun C, Yang F, Yang M, Fu Z, Yin Y, . Long non-coding RNA SNHG1 activates HOXA1 expression via sponging miR-193a-5p in breast cancer progression. . 12:10223-10234. https://doi.org/10.18632/aging.103123

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                TY  - JOUR
                AU  - Li, Jun 
                AU  - Zeng, Tianyu 
                AU  - Li, Wei 
                AU  - Wu, Hao 
                AU  - Sun, Chunxiao 
                AU  - Yang, Fan 
                AU  - Yang, Mengzhu 
                AU  - Fu, Ziyi 
                AU  - Yin, Yongmei 
                TI  - Long non-coding RNA SNHG1 activates HOXA1 expression via sponging miR-193a-5p in breast cancer progression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103123
                DO  - 10.18632/aging.103123
                SP  - 10223
                EP  - 10234
                PY  - 
                AB  - Breast cancer is the leading cause of cancer death in women worldwide. Long non-coding RNA small nucleolar RNA host gene 1 (SNHG1) has been reported to be involved in human diseases, including cancer. Here, we found that SNHG1 expression was significantly upregulated in human breast cancer tissues and cell lines. We explored the function of SNHG1 in breast cancer cells using in vitro and in vivo experiments and found that SNHG1 promotes breast cancer metastasis and proliferation. The potential molecular mechanism of SNHG1 in breast cancer cells may involve SNHG1 acting as a sponge of miR-193a-5p to activate the expression of the oncogene HOXA1. In summary, our study reveals a novel SNHG1/miR-193a-5p/HOXA1 competing endogenous RNA regulatory pathway in breast cancer progression and may provide new strategies for breast cancer therapy.
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miR-195-5p alleviates acute kidney injury through repression of inflammation and oxidative stress by targeting vascular endothelial growth factor A

Yong Xu, Wei Jiang, Lili Zhong, Hailun Li, Lin Bai, Xiaoling Chen, Yongtao Lin, Donghui Zheng,

https://doi.org/10.18632/aging.103160 pp 10235—10245

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Xu Y, Jiang W, Zhong L, Li H, Bai L, Chen X, Lin Y, Zheng D, . miR-195-5p alleviates acute kidney injury through repression of inflammation and oxidative stress by targeting vascular endothelial growth factor A. . 12:10235-10245. https://doi.org/10.18632/aging.103160

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                TY  - JOUR
                AU  - Xu, Yong 
                AU  - Jiang, Wei 
                AU  - Zhong, Lili 
                AU  - Li, Hailun 
                AU  - Bai, Lin 
                AU  - Chen, Xiaoling 
                AU  - Lin, Yongtao 
                AU  - Zheng, Donghui 
                TI  - miR-195-5p alleviates acute kidney injury through repression of inflammation and oxidative stress by targeting vascular endothelial growth factor A
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103160
                DO  - 10.18632/aging.103160
                SP  - 10235
                EP  - 10245
                PY  - 
                AB  - Acute kidney injury (AKI) is a common renal dysfunction. Renal ischemia-reperfusion (I/R) injury contributes to AKI progression. The microRNA miR-195-5p can act as a crucial tumor inhibitor in various cancers. However, the potential biological effects of miR-195-5p on AKI are not well-understood. We found that miR-195-5p levels were decreased in the serum samples of patients with AKI. Next, we determined miR-195-5p expression in the renal tissues of the rats and found that it was downregulated. Renal function was evaluated and confirmed using blood urea nitrogen and serum Cr levels. In parallel, the hypoxia-induced NRK-52E cell model was employed, and miR-195-5p was found to be markedly reduced under hypoxic conditions. Furthermore, miR-195-5p was modulated in NRK-52E cells. miR-195-5p induced NRK-52E cell proliferation and protected NRK-52E cells against hypoxia-triggered apoptosis. In an I/R mouse model, miR-195-5p alleviated renal injury triggered by I/R. In addition, oxidative stress and inflammatory factor concentrations were assessed using ELISA. The results showed that miR-195-5p mimicked attenuated oxidative stress induced by I/R injury and downregulated the protein expression of inflammatory factors. Moreover, we identified that vascular endothelial growth factor A (VEGFA) was a target gene of miR-195-5p, which could negatively regulate VEGFA expression in vitro. Inhibitors of miR-195-5p subsequently contributed to renal injury, which was reversed by VEGFA loss. In conclusion, miR-195-5p may repress AKI by targeting VEGFA.
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miR-623 suppresses cell proliferation, migration and invasion through direct inhibition of XRCC5 in breast cancer

Qing Li, Jiangtao Liu, Yanli Jia, Tingting Li, Mei Zhang,

https://doi.org/10.18632/aging.103182 pp 10246—10258

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Li Q, Liu J, Jia Y, Li T, Zhang M, . miR-623 suppresses cell proliferation, migration and invasion through direct inhibition of XRCC5 in breast cancer. . 12:10246-10258. https://doi.org/10.18632/aging.103182

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                TY  - JOUR
                AU  - Li, Qing 
                AU  - Liu, Jiangtao 
                AU  - Jia, Yanli 
                AU  - Li, Tingting 
                AU  - Zhang, Mei 
                TI  - miR-623 suppresses cell proliferation, migration and invasion through direct inhibition of XRCC5 in breast cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103182
                DO  - 10.18632/aging.103182
                SP  - 10246
                EP  - 10258
                PY  - 
                AB  - Background/Aims: MicroRNAs (miRNAs) are short, non-coding RNA molecules that control gene expression trough negative translational regulation. MiR-623 is a tumor suppressor, and it&#x2019;s function and mechanism in breast cancer has not been reported.Results: Exogenous overexpression of miR-623 suppressed cell proliferation, migration and invasion, meanwhile, but promoted cell apoptosis. MiR-623 knockdown displayed opposite results. Overexpression of miR-623 resulted in the downregulation of CDK4/6 as well as the inhibition of the phosphatidylinositol-3-kinase (PI3K)/Akt and Wnt/&#x3B2;-Catenin signaling pathways. MiR-623 knockdown displayed opposite results. Results of the reporter assay revealed that the luciferase activity was decreased in XRCC5-wt cells, suggesting that miR-623 could directly combine with 3&#x2019; UTR of XRCC5. MiR-623 significantly suppressed XRCC5 expression, which is critical for miR-623-induced proliferation and migration block in breast cancer cells.Conclusion: miR-623 suppressed cell proliferation, migration and invasion through downregulation of cyclin dependent kinases and inhibition of the phosphatidylinositol-3-kinase (PI3K)/Akt and Wnt/&#x3B2;-Catenin pathways by targeting XRCC5.Methods: miR-623 was either overexpressed in breast cancer cell lines through exogenous transfection or knocked down by specific siRNA. Cell proliferation, migration and invasion were examined using CCK-8, colony formation and transwell assay. The direct target of miR-623 was verified using luciferase reporter gene assay.
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Structural plasticity of the bilateral hippocampus in glioma patients

Taoyang Yuan, Jianyou Ying, Zhentao Zuo, Songbai Gui, Zhixian Gao, Guilin Li, Yazhuo Zhang, Chuzhong Li,

https://doi.org/10.18632/aging.103212 pp 10259—10274

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Yuan T, Ying J, Zuo Z, Gui S, Gao Z, Li G, Zhang Y, Li C, . Structural plasticity of the bilateral hippocampus in glioma patients. . 12:10259-10274. https://doi.org/10.18632/aging.103212

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                TY  - JOUR
                AU  - Yuan, Taoyang 
                AU  - Ying, Jianyou 
                AU  - Zuo, Zhentao 
                AU  - Gui, Songbai 
                AU  - Gao, Zhixian 
                AU  - Li, Guilin 
                AU  - Zhang, Yazhuo 
                AU  - Li, Chuzhong 
                TI  - Structural plasticity of the bilateral hippocampus in glioma patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103212
                DO  - 10.18632/aging.103212
                SP  - 10259
                EP  - 10274
                PY  - 
                AB  - This study investigates the structural plasticity and neuronal reaction of the hippocampus in glioma patient pre-surgery. Ninety-nine glioma patients without bilateral hippocampus involvement (low-grade, n=52; high-grade, n=47) and 80 healthy controls with 3D T1 images and resting-fMRI were included. Hippocampal volume and dynamic amplitude of low-frequency fluctuation (dALFF) were analyzed among groups. Relationships between hippocampal volume and clinical characteristics were assessed. We observed remote hippocampal volume increases in low- and high-grade glioma and a greater response of the ipsilateral hippocampus than the contralesional hippocampus. The bilateral hippocampal dALFF was significantly increased in high-grade glioma. Tumor-associated epilepsy and the IDH-1 mutation did not affect hippocampal volume in glioma patients. No significant relationship between hippocampal volume and age was observed in high-grade glioma. The Kaplan-Meier curve and log-rank test revealed that large hippocampal volume was associated with shorter overall survival (OS) compared with small hippocampal volume (p=0.007). Multivariate Cox regression analysis revealed that large hippocampal volume was an independent predictor of unfavorable OS (HR=3.597, 95% CI: 1.160-11.153, p=0.027) in high-grade glioma. Our findings suggest that the hippocampus has a remarkable degree of plasticity in response to pathological stimulation of glioma and that the hippocampal reaction to glioma may be related to tumor malignancy.
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UBE2T promotes glioblastoma invasion and migration via stabilizing GRP78 and regulating EMT

Peng Huang, Yuduo Guo, Zitong Zhao, Weihai Ning, Haoran Wang, Chunyu Gu, Mingshan Zhang, Yanming Qu, Hongwei Zhang, Yongmei Song,

https://doi.org/10.18632/aging.103239 pp 10275—10289

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Huang P, Guo Y, Zhao Z, Ning W, Wang H, Gu C, Zhang M, Qu Y, Zhang H, Song Y, . UBE2T promotes glioblastoma invasion and migration via stabilizing GRP78 and regulating EMT. . 12:10275-10289. https://doi.org/10.18632/aging.103239

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                TY  - JOUR
                AU  - Huang, Peng 
                AU  - Guo, Yuduo 
                AU  - Zhao, Zitong 
                AU  - Ning, Weihai 
                AU  - Wang, Haoran 
                AU  - Gu, Chunyu 
                AU  - Zhang, Mingshan 
                AU  - Qu, Yanming 
                AU  - Zhang, Hongwei 
                AU  - Song, Yongmei 
                TI  - UBE2T promotes glioblastoma invasion and migration via stabilizing GRP78 and regulating EMT
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103239
                DO  - 10.18632/aging.103239
                SP  - 10275
                EP  - 10289
                PY  - 
                AB  - Glioblastoma (GBM) generally has a dismal prognosis, and it is associated with a poor quality of life as the disease progresses. However, the development of effective therapies for GBM has been deficient. Ubiquitin-conjugating enzyme E2T (UBE2T) is a member of the E2 family in the ubiquitin-proteasome pathway and a vital regulator of tumour progression, but its role in GBM is unclear. In this study, we aimed to clarify the role of UBE2T in GBM. Bioinformatics analysis identified UBE2T as an independent risk factor for gliomas. Immunohistochemistry was used to measure UBE2T expression in GBM and normal tissue samples obtained from patients with GBM. The effects of UBE2T on GBM cell invasion and migration were analysed using the Transwell assay. BALB/c nude mice were used for the in vivo assays. Immunoblotting and immunoprecipitation were performed to determine the molecular mechanisms. UBE2T was highly expressed in GBM tissues, and its expression was linked to a poor prognosis. In vitro, depletion of UBE2T significantly suppressed cell invasion and migration. Moreover, UBE2T depletion suppressed the growth of GBM subcutaneous tumours in vivo. Further experiments revealed that UBE2T suppressed invasion and migration by regulating epithelial- mesenchymal transition (EMT) via stabilising GRP78 in GBM cells. We uncovered a novel UBE2T/GRP78/EMT regulatory axis that modulates the malignant progression and recurrence of GBM, indicating that the axis might be a valuable therapeutic target.
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Interactive effect of MTHFR C677T polymorphism and sex on symptoms and cognitive functions in Chinese patients with chronic schizophrenia

Jie Gao, Mei Hong Xiu, Dian Ying Liu, Chang Wei Wei, Xiangyang Zhang,

https://doi.org/10.18632/aging.103248 pp 10290—10299

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Gao J, Xiu MH, Liu DY, Wei CW, Zhang X, . Interactive effect of MTHFR C677T polymorphism and sex on symptoms and cognitive functions in Chinese patients with chronic schizophrenia. . 12:10290-10299. https://doi.org/10.18632/aging.103248

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 TY - JOUR
 AU - Gao, Jie 
 AU - Xiu, Mei Hong 
 AU - Liu, Dian Ying 
 AU - Wei, Chang Wei 
 AU - Zhang, Xiangyang 
 TI - Interactive effect of MTHFR C677T polymorphism and sex on symptoms and cognitive functions in Chinese patients with chronic schizophrenia
 JO - 
 JA - 
 VL - 12
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103248
 DO - 10.18632/aging.103248
 SP - 10290
 EP - 10299
 PY - 
 AB - The etiology of schizophrenia is still unknown, and the MTHFR gene has been shown to be associated with SCZ. Previous studies have shown that patients with schizophrenia exhibit sex differences in symptoms and cognitive function. However, no study has been conducted to investigate the sex difference in the association between C677T polymorphism and symptoms and cognitive impairment in Chinese patients with schizophrenia. The C677T polymorphism was genotyped in 957 patients with schizophrenia and 576 controls. Patients were also rated on the Positive and Negative Syndrome Scale (PANSS) and the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). The results showed that there were significant differences in MTHFR C677T genotype and allele distributions between male patients and male controls (both p&lt;0.05), while there was no significant difference between female patients and female controls (both p&gt;0.05). Further analysis showed that there were significant sex differences in the association between C677T genotype and negative symptoms, immediate memory or attention index score in schizophrenia (p&lt;0.05). This study suggests that the complex interactive effect between MTHFR C677T polymorphism and sex plays an important role in some clinical characteristics of patients with schizophrenia.
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Alterations in glycolytic/cholesterogenic gene expression in hepatocellular carcinoma

Jianwen Jiang, Qiuxian Zheng, Weiwei Zhu, Xinhua Chen, Haifeng Lu, Deying Chen, Hua Zhang, Min Shao, Lin Zhou, Shusen Zheng,

https://doi.org/10.18632/aging.103254 pp 10300—10316

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Jiang J, Zheng Q, Zhu W, Chen X, Lu H, Chen D, Zhang H, Shao M, Zhou L, Zheng S, . Alterations in glycolytic/cholesterogenic gene expression in hepatocellular carcinoma. . 12:10300-10316. https://doi.org/10.18632/aging.103254

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                TY  - JOUR
                AU  - Jiang, Jianwen 
                AU  - Zheng, Qiuxian 
                AU  - Zhu, Weiwei 
                AU  - Chen, Xinhua 
                AU  - Lu, Haifeng 
                AU  - Chen, Deying 
                AU  - Zhang, Hua 
                AU  - Shao, Min 
                AU  - Zhou, Lin 
                AU  - Zheng, Shusen 
                TI  - Alterations in glycolytic/cholesterogenic gene expression in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103254
                DO  - 10.18632/aging.103254
                SP  - 10300
                EP  - 10316
                PY  - 
                AB  - Metabolic reprogramming is a hallmark of tumors, including hepatocellular carcinoma (HCC). We used data from The Cancer Genome Atlas and the International Cancer Genome Consortium to assess the alterations in glycolytic and cholesterogenic genes in HCC and to determine their association with clinical features in HCC patients. Based on the gene expression profiles from these databases, we established four subtypes of HCC: cholesterogenic, glycolytic, mixed, and quiescent. The prognosis of the cholesterogenic subgroup was poorer than that of the glycolytic group. Tumors in the glycolytic group were more sensitive to chemotherapy. We also explored the relationships between these metabolic subtypes and previously established HCC subgroups. Glycolytic gene expression correlated strongly with poorer prognostic gene expression in the Hoshida classification of HCC. Whole-genome analyses indicated that aberrant amplification of TP53 and MYC in HCC were associated with abnormal anabolic cholesterol metabolism. The mRNA levels of mitochondrial pyruvate carriers 1 and 2 differed among the HCC metabolic subtypes. In a bioinformatics analysis we identified genomic characteristics of tumor metabolism that varied among different cancer types. These findings demonstrate that metabolic subtypes may be valuable prognostic indicators in HCC patients.
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Nomogram for the prediction of diabetic nephropathy risk among patients with type 2 diabetes mellitus based on a questionnaire and biochemical indicators: a retrospective study

Yuhong Hu, Rong Shi, Ruohui Mo, Fan Hu,

https://doi.org/10.18632/aging.103259 pp 10317—10336

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Hu Y, Shi R, Mo R, Hu F, . Nomogram for the prediction of diabetic nephropathy risk among patients with type 2 diabetes mellitus based on a questionnaire and biochemical indicators: a retrospective study. . 12:10317-10336. https://doi.org/10.18632/aging.103259

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                TY  - JOUR
                AU  - Hu, Yuhong 
                AU  - Shi, Rong 
                AU  - Mo, Ruohui 
                AU  - Hu, Fan 
                TI  - Nomogram for the prediction of diabetic nephropathy risk among patients with type 2 diabetes mellitus based on a questionnaire and biochemical indicators: a retrospective study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103259
                DO  - 10.18632/aging.103259
                SP  - 10317
                EP  - 10336
                PY  - 
                AB  - Purpose: Develop a diabetic nephropathy incidence risk nomogram in a Chinese population with type 2 diabetes mellitus.Results: Predictors included systolic blood pressure, diastolic blood pressure, fasting blood glucose, glycosylated hemoglobin A1c, total triglycerides, serum creatinine, blood urea nitrogen and body mass index. The model displayed medium predictive power with a C-index of 0.744 and an area under curve of 0.744. Internal verification of C-index reached 0.737. The decision curve analysis showed the risk threshold was 20%. The value of net reclassification improvement and integrated discrimination improvement were 0.131, 0.05, and that the nomogram could be applied in clinical practice.Conclusion: Diabetic nephropathy incidence risk nomogram incorporating 8 features is useful to predict diabetic nephropathy incidence risk in type 2 diabetes mellitus patients.Methods: Questionnaires, physical examinations and biochemical tests were performed on 3489 T2DM patients in six communities in Shanghai. LASSO regression was used to optimize feature selection by running cyclic coordinate descent. Logistic regression analysis was applied to build a prediction model incorporating the selected features. The C-index, calibration plot, curve analysis, forest plot, net reclassification improvement, integrated discrimination improvement and internal validation were used to validate the discrimination, calibration and clinical usefulness of the model.
                ER  -

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Altered expression of fibroblast activation protein-α (FAP) in colorectal adenoma-carcinoma sequence and in lymph node and liver metastases

Jon Danel Solano-Iturri, Maider Beitia, Peio Errarte, Julio Calvete-Candenas, María C. Etxezarraga, Alberto Loizate, Enrique Echevarria, Iker Badiola, Gorka Larrinaga,

https://doi.org/10.18632/aging.103261 pp 10337—10358

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Solano-Iturri JD, Beitia M, Errarte P, Calvete-Candenas J, Etxezarraga MC, Loizate A, Echevarria E, Badiola I, Larrinaga G, . Altered expression of fibroblast activation protein-α (FAP) in colorectal adenoma-carcinoma sequence and in lymph node and liver metastases. . 12:10337-10358. https://doi.org/10.18632/aging.103261

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                TY  - JOUR
                AU  - Solano-Iturri, Jon Danel 
                AU  - Beitia, Maider 
                AU  - Errarte, Peio 
                AU  - Calvete-Candenas, Julio 
                AU  - Etxezarraga, María C. 
                AU  - Loizate, Alberto 
                AU  - Echevarria, Enrique 
                AU  - Badiola, Iker 
                AU  - Larrinaga, Gorka 
                TI  - Altered expression of fibroblast activation protein-α (FAP) in colorectal adenoma-carcinoma sequence and in lymph node and liver metastases
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103261
                DO  - 10.18632/aging.103261
                SP  - 10337
                EP  - 10358
                PY  - 
                AB  - Colorectal cancer (CRC) is a major health problem in elderly people because of its high incidence and high mortality rate. Despite early screening programs, more than half of CRC patients are diagnosed at advanced stages. Fibroblast activation protein-&#x3B1; (FAP) expression in cancer-associated fibroblasts (CAFs) has been associated with a higher risk of metastases and poor survival. Here, we have analyzed the immunohistochemical expression of FAP in 41 adenoma-carcinoma sequences. In addition, FAP expression was analyzed individually and in combination with &#x3B2;-catenin (BCAT), CD44 and Cyclin-D1 expression in primary tumors and in their corresponding lymph node and liver metastases (n=294). Finally, soluble FAP (sFAP) levels in plasma from CRC patients (n=127) were also analyzed by ELISA. FAP was expressed only in CRC tissue and its expression level was found to be higher in tumors exhibiting deeper local invasion and poorer cancer cell differentiation. FAP and concomitant nuclear BCAT expression in cancer cells at the infiltrating front of primary tumors and in lymph node metastases was independently associated with 5- and 10-year cancer specific and disease-free survival. Moreover, lower sFAP levels correlated with poorer survival. These findings support the potential importance of FAP as a biomarker of CRC development and progression.
                ER  -

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Resveratrol promotes osteogenesis and alleviates osteoporosis by inhibiting p53

Tao Yu, Zaiyan Wang, Xiaomeng You, Haichao Zhou, Wenbao He, Bing Li, Jiang Xia, Hui Zhu, Youguang Zhao, Guangrong Yu, Yuan Xiong, Yunfeng Yang,

https://doi.org/10.18632/aging.103262 pp 10359—10369

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Yu T, Wang Z, You X, Zhou H, He W, Li B, Xia J, Zhu H, Zhao Y, Yu G, Xiong Y, Yang Y, . Resveratrol promotes osteogenesis and alleviates osteoporosis by inhibiting p53. . 12:10359-10369. https://doi.org/10.18632/aging.103262

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                TY  - JOUR
                AU  - Yu, Tao 
                AU  - Wang, Zaiyan 
                AU  - You, Xiaomeng 
                AU  - Zhou, Haichao 
                AU  - He, Wenbao 
                AU  - Li, Bing 
                AU  - Xia, Jiang 
                AU  - Zhu, Hui 
                AU  - Zhao, Youguang 
                AU  - Yu, Guangrong 
                AU  - Xiong, Yuan 
                AU  - Yang, Yunfeng 
                TI  - Resveratrol promotes osteogenesis and alleviates osteoporosis by inhibiting p53
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103262
                DO  - 10.18632/aging.103262
                SP  - 10359
                EP  - 10369
                PY  - 
                AB  - Although osteoporosis is one of the most common chronic age-related diseases, there is currently no gold standard for treatment. Evidence suggests resveratrol, a natural polyphenolic compound, may be helpful in the treatment of osteoporosis and other diseases. However, the molecular mechanisms underlying the anti-osteoporotic effects of resveratrol remain largely unknown. In the present study, KEGG pathway enrichment analysis of resveratrol-targeted genes identified 33 associated pathways, 12 of which were also involved in osteoporosis. In particular, the MDM2/p53 signaling pathway was identified as a potential key pathway among the shared pathways. In vitro experiments indicated that MDM2-mediated p53 degradation induced osteoblast differentiation, and resveratrol could partially reverse p53-dependent inhibition of osteogenic differentiation. These findings suggest resveratrol may alleviate osteoporosis at least in part by modulating the MDM2/p53 signaling pathway.
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Keap1-Nrf2 signaling activation by Bardoxolone-methyl ameliorates high glucose-induced oxidative injury in human umbilical vein endothelial cells

Jing-Lei Yang, Meng-Yue Sun, Qi Yuan, Shan Tang, Mei-Juan Dong, Ri-Dong Zhang, Yuan-Yuan Liu, Li Mao,

https://doi.org/10.18632/aging.103263 pp 10370—10380

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Yang J, Sun M, Yuan Q, Tang S, Dong M, Zhang R, Liu Y, Mao L, . Keap1-Nrf2 signaling activation by Bardoxolone-methyl ameliorates high glucose-induced oxidative injury in human umbilical vein endothelial cells. . 12:10370-10380. https://doi.org/10.18632/aging.103263

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                TY  - JOUR
                AU  - Yang, Jing-Lei 
                AU  - Sun, Meng-Yue 
                AU  - Yuan, Qi 
                AU  - Tang, Shan 
                AU  - Dong, Mei-Juan 
                AU  - Zhang, Ri-Dong 
                AU  - Liu, Yuan-Yuan 
                AU  - Mao, Li 
                TI  - Keap1-Nrf2 signaling activation by Bardoxolone-methyl ameliorates high glucose-induced oxidative injury in human umbilical vein endothelial cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103263
                DO  - 10.18632/aging.103263
                SP  - 10370
                EP  - 10380
                PY  - 
                AB  - In cultured human umbilical vein endothelial cells (HUVECs) high glucose (HG) stimulation will lead to significant cell death. Bardoxolone-methyl (BARD) is a NF-E2 p45-related factor 2 (Nrf2) agonist. In this study we show that BARD, at only nM concentrations, activated Nrf2 signaling in HUVECs. BARD induced Keap1-Nrf2 disassociation, Nrf2 protein stabilization and nuclear translocation, increasing expression of antioxidant response element (ARE) genes. BARD pretreatment in HUVECs inhibited HG-induced reactive oxygen species production, oxidative injury and cell apoptosis. Nrf2 shRNA or knockout (using a CRISPR/Cas9 construct) reversed BARD-induced cytoprotection in HG-stimulated HUVECs. Conversely, forced activation of Nrf2 cascade by Keap1 shRNA mimicked BARD&#x2019;s activity and protected HUVECs from HG. Importantly, BARD failed to offer further cytoprotection against HG in the Keap1-silened HUVECs. Taken together, Keap1-Nrf2 cascade activation by BARD protects HUVECs from HG-induced oxidative injury.
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High circ-SEC31A expression predicts unfavorable prognoses in non-small cell lung cancer by regulating the miR-520a-5p/GOT-2 axis

Mingming Jin, Chunzi Shi, Qian Hua, Tian Li, Chen Yang, Yue Wu, Licong Zhao, Hao Yang, Jiaqi Zhang, Cheng Hu, Gang Huang,

https://doi.org/10.18632/aging.103264 pp 10381—10397

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Jin M, Shi C, Hua Q, Li T, Yang C, Wu Y, Zhao L, Yang H, Zhang J, Hu C, Huang G, . High circ-SEC31A expression predicts unfavorable prognoses in non-small cell lung cancer by regulating the miR-520a-5p/GOT-2 axis. . 12:10381-10397. https://doi.org/10.18632/aging.103264

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                TY  - JOUR
                AU  - Jin, Mingming 
                AU  - Shi, Chunzi 
                AU  - Hua, Qian 
                AU  - Li, Tian 
                AU  - Yang, Chen 
                AU  - Wu, Yue 
                AU  - Zhao, Licong 
                AU  - Yang, Hao 
                AU  - Zhang, Jiaqi 
                AU  - Hu, Cheng 
                AU  - Huang, Gang 
                TI  - High circ-SEC31A expression predicts unfavorable prognoses in non-small cell lung cancer by regulating the miR-520a-5p/GOT-2 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103264
                DO  - 10.18632/aging.103264
                SP  - 10381
                EP  - 10397
                PY  - 
                AB  - Dysregulation of circular RNAs (circRNAs) has recently been shown to play important regulatory roles in cancer development and progression, including non-small cell lung cancer (NSCLC). However, the roles of most circRNAs in NSCLC are still unknown. In this study, we found that hsa_circ_0001421 (circ-SEC31A) was upregulated in NSCLC tissues and cell lines. Increased circ-SEC31A expression in NSCLC was significantly correlated with malignant characteristics and served as an independent risk factor for the post-surgical overall survival of NSCLC patients. Reduced circ-SEC31A expression in NSCLC decreased tumor cell proliferation, migration, invasion, and malate-aspartate metabolism. Mechanistically, we demonstrated that silencing circ-SEC31A downregulated GOT-2 expression by relieving the sponging effect of miR-520a-5p, which resulted in significantly reduced malate-aspartate metabolism in NSCLC cells. Taken together, these results revealed the important role of circ-SEC31A in the proliferation, migration, invasion, and metabolic regulation of NSCLC cells, providing a new perspective on circRNAs in NSCLC progression.
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Testosterone enhances mitochondrial complex V function in the substantia nigra of aged male rats

Tianyun Zhang, Yu Wang, Yunxiao Kang, Li Wang, Hui Zhao, Xiaoming Ji, Yuanxiang Huang, Wensheng Yan, Rui Cui, Guoliang Zhang, Geming Shi,

https://doi.org/10.18632/aging.103265 pp 10398—10414

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Zhang T, Wang Y, Kang Y, Wang L, Zhao H, Ji X, Huang Y, Yan W, Cui R, Zhang G, Shi G, . Testosterone enhances mitochondrial complex V function in the substantia nigra of aged male rats. . 12:10398-10414. https://doi.org/10.18632/aging.103265

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                TY  - JOUR
                AU  - Zhang, Tianyun 
                AU  - Wang, Yu 
                AU  - Kang, Yunxiao 
                AU  - Wang, Li 
                AU  - Zhao, Hui 
                AU  - Ji, Xiaoming 
                AU  - Huang, Yuanxiang 
                AU  - Yan, Wensheng 
                AU  - Cui, Rui 
                AU  - Zhang, Guoliang 
                AU  - Shi, Geming 
                TI  - Testosterone enhances mitochondrial complex V function in the substantia nigra of aged male rats
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103265
                DO  - 10.18632/aging.103265
                SP  - 10398
                EP  - 10414
                PY  - 
                AB  - Deficits in coordinated motor behavior and mitochondrial complex V activity have been observed in aged males. Testosterone supplementation can improve coordinated motor behavior in aged males. We investigated the effects of testosterone supplementation on mitochondrial complex V function in the substantia nigra (a brain region that regulates motor activity) in aged male rats. These rats exhibited diminished ATP levels, attenuated mitochondrial complex V activity, and reduced expression of 3 of the 17 mitochondrial complex V subunits (ATP6, ATP8 and ATP5C1) in the substantia nigra. Testosterone supplementation increased ATP levels, mitochondrial complex V activity, and ATP6, ATP8 and ATP5C1 expression in the substantia nigra of the rats. Conversely, orchiectomy reduced mitochondrial complex V activity, downregulated ATP6 and ATP8 expression, and upregulated ATP5C1, ATP5I and ATP5L expression in the substantia nigra. Testosterone replacement reversed those effects. Thus, testosterone enhanced mitochondrial complex V function in the substantia nigra of aged male rats by upregulating ATP6 and ATP8. As potential testosterone targets, these two subunits may to some degree maintain nigrostriatal dopaminergic function in aged males.
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CHK2 is essential for spindle assembly and DNA repair during the first cleavage of mouse embryos

Xiao-Han Li, Wen-Jing Li, Jia-Qian Ju, Meng-Hao Pan, Yao Xu, Ming-Hong Sun, Mo Li, Shao-Chen Sun,

https://doi.org/10.18632/aging.103267 pp 10415—10426

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Li X, Li W, Ju J, Pan M, Xu Y, Sun M, Li M, Sun S, . CHK2 is essential for spindle assembly and DNA repair during the first cleavage of mouse embryos. . 12:10415-10426. https://doi.org/10.18632/aging.103267

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                TY  - JOUR
                AU  - Li, Xiao-Han 
                AU  - Li, Wen-Jing 
                AU  - Ju, Jia-Qian 
                AU  - Pan, Meng-Hao 
                AU  - Xu, Yao 
                AU  - Sun, Ming-Hong 
                AU  - Li, Mo 
                AU  - Sun, Shao-Chen 
                TI  - CHK2 is essential for spindle assembly and DNA repair during the first cleavage of mouse embryos
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103267
                DO  - 10.18632/aging.103267
                SP  - 10415
                EP  - 10426
                PY  - 
                AB  - The quality of the early embryo is critical for embryonic development and implantation. Errors during cleavage lead to aneuploidy in embryos. As a cell cycle checkpoint protein, CHK2 participates in DNA replication, cell cycle arrest and spindle assembly. However, the functions of CHK2 in early development of the mouse embryo remain largely unknown. In this study, we show that CHK2 is localized on the spindle in metaphase and mainly accumulates at spindle poles in anaphase/telophase during the first cleavage of the mouse embryo. CHK2 inhibition led to cleavage failure in early embryonic development, accompanied by abnormal spindle assembly and misaligned chromosomes. Moreover, the loss of CHK2 activity increased the level of cellular DNA damage, which resulted in oxidative stress. Then, apoptosis and autophagy were found to be active in these embryos. In summary, our results suggest that CHK2 is an essential regulator of spindle assembly and DNA repair during early embryonic development in mice.
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LncRNA PVT1 promotes exosome secretion through YKT6, RAB7, and VAMP3 in pancreatic cancer

Chengming Sun, Peng Wang, Wei Dong, Haishi Liu, Jianmin Sun, Liang Zhao,

https://doi.org/10.18632/aging.103268 pp 10427—10440

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Sun C, Wang P, Dong W, Liu H, Sun J, Zhao L, . LncRNA PVT1 promotes exosome secretion through YKT6, RAB7, and VAMP3 in pancreatic cancer. . 12:10427-10440. https://doi.org/10.18632/aging.103268

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                TY  - JOUR
                AU  - Sun, Chengming 
                AU  - Wang, Peng 
                AU  - Dong, Wei 
                AU  - Liu, Haishi 
                AU  - Sun, Jianmin 
                AU  - Zhao, Liang 
                TI  - LncRNA PVT1 promotes exosome secretion through YKT6, RAB7, and VAMP3 in pancreatic cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103268
                DO  - 10.18632/aging.103268
                SP  - 10427
                EP  - 10440
                PY  - 
                AB  - Pancreatic cancer (PC) is one of the deadliest cancers worldwide. Cancer cells secrete excessive numbers of exosomes that play essential roles in tumorigenesis. Long non-coding RNAs (lncRNAs) are essential non-coding RNAs for cancer progression. However, the role of lncRNA plasmacytoma variant translocation 1 (PVT1) in exosome secretion of PC remains to be comprehensively investigated. Thus, nanoparticle tracking analysis and transmission electron microscopy were performed to determine exosome secretion. Confocal microscopy, western blots, real-time PCR, immunofluorescence, pull-down and RNA immunoprecipitation assays, and rescue experiments were applied to investigate the mechanism underlying the role of PVT1 in exosome secretion. The results showed that PVT1 was upregulated in PC cells, along with increased levels of YKT6 v-SNARE homolog (YKT6), ras-related protein Rab-7 (RAB7), and vesicle-associated membrane protein 3 (VAMP3). Also, PVT1 promoted the transportation of multivesicular bodies (MVBs) towards the plasma membrane. In addition, PVT1 promoted the docking of MVBs by altering RAB7 expression and localization. Moreover, PVT1 promoted the fusion of MVBs with the plasma membrane through regulating YKT6 and VAMP3 colocalization and the palmitoylation of YKT6. Taken together, the results suggest that PVT1 promoted exosome secretion of PC cells and thus, can expand the understanding of PVT1 in tumor biology.
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LncRNA SNHG7 promotes cardiac remodeling by upregulating ROCK1 via sponging miR-34-5p

Jie Wang, Shouwen Zhang, Xinhua Li, Maolei Gong,

https://doi.org/10.18632/aging.103269 pp 10441—10456

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Wang J, Zhang S, Li X, Gong M, . LncRNA SNHG7 promotes cardiac remodeling by upregulating ROCK1 via sponging miR-34-5p. . 12:10441-10456. https://doi.org/10.18632/aging.103269

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                TY  - JOUR
                AU  - Wang, Jie 
                AU  - Zhang, Shouwen 
                AU  - Li, Xinhua 
                AU  - Gong, Maolei 
                TI  - LncRNA SNHG7 promotes cardiac remodeling by upregulating ROCK1 via sponging miR-34-5p
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103269
                DO  - 10.18632/aging.103269
                SP  - 10441
                EP  - 10456
                PY  - 
                AB  - Previous studies have shown that lncRNA small nuclear RNA host gene 7 (lncRNA SNHG7) played an important role in cancer progression. However, the role of lncRNA SNHG7 in cardiac fibrosis is still poorly understood. In this study, the results of quantitative real time polymerase chain reaction (qRT-PCR) analysis showed that lncRNA SNHG7 was over expressed in the infarcted and peri-infarcted area in the left ventricle after MI in mice. Western blot analysis showed that knockdown of SNHG7 decreased the expression of collagen type 1 (Col1)and &#x3B1;-smooth muscle actin (&#x3B1;-SMA). Echocardiographic study suggested that inhibition of SNHG7 improved cardiac function after MI in mice. Luciferase assay indicated SNHG7 could act as a competing endogenous RNA (ceRNA) by sponging miR-34-5p. The MTT cell proliferation assay and 5-ethynyl-2&#x2019;-deoxyuridine (EdU) labelling assay revealed that co-transfection of SNHG7 and miR-34-5p inhibited cell viability and proliferation of cardiac fibroblasts (CF). All the results indicated that lncRNA SNHG7 could promote cardiac fibrosis via targeting miR-34-5p through acting as a ceRNA in mice after MI. Silencing of SNHG7 could attenuate deposition of collagens and improve cardiac function. miR-34-5p could suppress the fibrogenesis of CF by targeting ROCK1 and abolish SNHG7-induced CF proliferation and fibroblast-to-myofibroblast transition.
                ER  -

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Ellagic acid protects mice against sleep deprivation-induced memory impairment and anxiety by inhibiting TLR4 and activating Nrf2

Wenjun Wang, Liudi Yang, Tianlong Liu, Jingwen Wang, Aidong Wen, Yi Ding,

https://doi.org/10.18632/aging.103270 pp 10457—10472

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Wang W, Yang L, Liu T, Wang J, Wen A, Ding Y, . Ellagic acid protects mice against sleep deprivation-induced memory impairment and anxiety by inhibiting TLR4 and activating Nrf2. . 12:10457-10472. https://doi.org/10.18632/aging.103270

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                TY  - JOUR
                AU  - Wang, Wenjun 
                AU  - Yang, Liudi 
                AU  - Liu, Tianlong 
                AU  - Wang, Jingwen 
                AU  - Wen, Aidong 
                AU  - Ding, Yi 
                TI  - Ellagic acid protects mice against sleep deprivation-induced memory impairment and anxiety by inhibiting TLR4 and activating Nrf2
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103270
                DO  - 10.18632/aging.103270
                SP  - 10457
                EP  - 10472
                PY  - 
                AB  - Sleep disorder has become a prevalent issue in current society and is connected with the deterioration of neurobehaviors such as mood, cognition and memory. Ellagic acid (EA) is a phenolic phytoconstituent extracted from grains and fruits that has potent neuroprotective properties. This research aimed to study the alleviative effect and mechanism of EA on memory impairment and anxiety caused by sleep deprivation (SD). EA ameliorated behavioral abnormalities in SD mice, associated with increased dendritic spine density, and reduced shrinkage and loss of hippocampal neurons. EA reduced the inflammatory response and oxidative stress injury caused by SD, which may be related to activation of the Nrf2/HO-1 pathway and mitigation of the TLR4-induced inflammatory response. In addition, EA significantly reduced the mortality and ROS levels in glutamate (Glu)-induced hippocampal neuron injury, and these effects of EA were enhanced in TLR4 siRNA-transfected neurons. However, knockdown of Nrf2 dramatically restrained the protective impact of EA on Glu-induced toxicity. Taken together, EA alleviated memory impairment and anxiety in sleep-deprived mice potentially by inhibiting TLR4 and activating Nrf2. Our findings suggested that EA may be a promising nutraceutical ingredient to prevent cognitive impairment and anxiety caused by sleep loss.
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p53 plays a central role in the development of osteoporosis

Tao Yu, Xiaomeng You, Haichao Zhou, Alex Kang, Wenbao He, Zihua Li, Bing Li, Jiang Xia, Hui Zhu, Youguang Zhao, Guangrong Yu, Yuan Xiong, Yunfeng Yang,

https://doi.org/10.18632/aging.103271 pp 10473—10487

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Yu T, You X, Zhou H, Kang A, He W, Li Z, Li B, Xia J, Zhu H, Zhao Y, Yu G, Xiong Y, Yang Y, . p53 plays a central role in the development of osteoporosis. . 12:10473-10487. https://doi.org/10.18632/aging.103271

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                TY  - JOUR
                AU  - Yu, Tao 
                AU  - You, Xiaomeng 
                AU  - Zhou, Haichao 
                AU  - Kang, Alex 
                AU  - He, Wenbao 
                AU  - Li, Zihua 
                AU  - Li, Bing 
                AU  - Xia, Jiang 
                AU  - Zhu, Hui 
                AU  - Zhao, Youguang 
                AU  - Yu, Guangrong 
                AU  - Xiong, Yuan 
                AU  - Yang, Yunfeng 
                TI  - p53 plays a central role in the development of osteoporosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103271
                DO  - 10.18632/aging.103271
                SP  - 10473
                EP  - 10487
                PY  - 
                AB  - Osteoporosis is a metabolic disease affecting 40% of postmenopausal women. It is characterized by decreased bone mass per unit volume and increased risk of fracture. We investigated the molecular mechanism underlying osteoporosis by identifying the genes involved in its development. Osteoporosis-related genes were identified by analyzing RNA microarray data in the GEO database to detect genes differentially expressed in osteoporotic and healthy individuals. Enrichment and protein interaction analyses carried out to identify the hub genes among the deferentially expressed genes revealed TP53, MAPK1, CASP3, CTNNB1, CCND1, NOTCH1, CDK1, IGF1, ERBB2, CYCS to be the top 10 hub genes. In addition, p53 had the highest degree score in the protein-protein interaction network. In vivo and in vitro experiments showed that TP53 gene expression and serum p53 levels were upregulated in osteoporotic patients and a mouse osteoporosis model. The elevated p53 levels were associated with decreases in bone mass, which could be partially reversed by knocking down p53. These findings suggest p53 may play a central role in the development of osteoporosis.
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Overexpression of hsa_circ_0136666 predicts poor prognosis and initiates osteosarcoma tumorigenesis through miR-593-3p/ZEB2 pathway

Chao Zhang, Haibo Zhou, Kaizhen Yuan, Raoying Xie, Chun Chen,

https://doi.org/10.18632/aging.103273 pp 10488—10496

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Zhang C, Zhou H, Yuan K, Xie R, Chen C, . Overexpression of hsa_circ_0136666 predicts poor prognosis and initiates osteosarcoma tumorigenesis through miR-593-3p/ZEB2 pathway. . 12:10488-10496. https://doi.org/10.18632/aging.103273

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                TY  - JOUR
                AU  - Zhang, Chao 
                AU  - Zhou, Haibo 
                AU  - Yuan, Kaizhen 
                AU  - Xie, Raoying 
                AU  - Chen, Chun 
                TI  - Overexpression of hsa_circ_0136666 predicts poor prognosis and initiates osteosarcoma tumorigenesis through miR-593-3p/ZEB2 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103273
                DO  - 10.18632/aging.103273
                SP  - 10488
                EP  - 10496
                PY  - 
                AB  - Background: Osteosarcoma (OS) is a type of malignant bone tumor with a growing incidence. Increasing studies indicate circular RNA (circRNA) has a vital function in tumorigenesis. Yet, how circRNA regulates OS development is not clear. In the present work, we aimed to investigate the roles of hsa_circ_0136666 in OS progression.Results: hsa_circ_0136666 was shown to be upregulated in OS and correlated with advanced stage and poor prognosis. Functional investigation using CCK8, colony formation assay and Transwell assay demonstrated that hsa_circ_0136666 promoted OS proliferation, migration and invasion, but inhibited cell death. Additionally, we identified hsa_circ_0136666 was a molecular sponge for miR-593-3p to facilitate ZEB2 expression. MiR-593-3p and ZEB2 were inversely expressed in OS tissues. And hsa_circ_0136666 exerts oncogenic roles in OS relying on miR-593-3p and ZEB2.Conclusion: Our results demonstrate the involvement of hsa_circ_0136666 in regulating OS tumorigenesis and it may be a therapeutic target.Methods: The expression of hsa_circ_0136666 was analyzed by qRT-PCR in OS tissues and cell lines. Proliferation was measured via CCK8 and colony formation assays. Migration and invasion were determined through Transwell assay. Luciferase reporter assay was utilized to determine the interaction between hsa_circ_0136666 and miR-593-3p or between miR-593-3p and ZEB2. Animal experiment was performed to investigate the role of hsa_circ_0136666 in vivo.
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Both objective and paradoxical insomnia elicit a stress response involving mitokine production

Morena Martucci, Maria Conte, Rita Ostan, Antonio Chiariello, Filomena Miele, Claudio Franceschi, Stefano Salvioli, Aurelia Santoro, Federica Provini,

https://doi.org/10.18632/aging.103274 pp 10497—10505

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Martucci M, Conte M, Ostan R, Chiariello A, Miele F, Franceschi C, Salvioli S, Santoro A, Provini F, . Both objective and paradoxical insomnia elicit a stress response involving mitokine production. . 12:10497-10505. https://doi.org/10.18632/aging.103274

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                TY  - JOUR
                AU  - Martucci, Morena 
                AU  - Conte, Maria 
                AU  - Ostan, Rita 
                AU  - Chiariello, Antonio 
                AU  - Miele, Filomena 
                AU  - Franceschi, Claudio 
                AU  - Salvioli, Stefano 
                AU  - Santoro, Aurelia 
                AU  - Provini, Federica 
                TI  - Both objective and paradoxical insomnia elicit a stress response involving mitokine production
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103274
                DO  - 10.18632/aging.103274
                SP  - 10497
                EP  - 10505
                PY  - 
                AB  - Chronic insomnia is the most common sleep disorder in the elderly population. From 9 to 50% of patients suffer of paradoxical insomnia, with the same symptoms and ailments, though characterized by normal sleep patterns. We have investigated the level of parameters related to stress in a group of post-menopausal female patients (age range 55-70 years) suffering by either objective or paradoxical insomnia, in particular we have measured 24-hours urinary cortisol, allostatic load index, Perceived Stress Scale (PSS) score, and, for the first time, mitokines (mitochondrial stress response molecules) such as FGF21, GDF15 and Humanin (HN). Results show that the two groups are different as far as sleep efficiency score, as expected, but not for stress parameters, that in some cases resulted within the normality range, although quite close to the top threshold (such as cortisol) or much higher with respect to normality ranges (such as PSS). Therefore, the consequences of paradoxical insomnia on the expression of these parameters are the same as objective insomnia. As far as the level of mitokines, we showed that FGF21 and HN in particular resulted altered (decreased and increased, respectively) with respect to control population, however with no difference between the two groups of patients.
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Modification of graphene oxide by angiopep-2 enhances anti-glioma efficiency of the nanoscaled delivery system for doxorubicin

Yue Zhao, Hang Yin, Xiaoyu Zhang,

https://doi.org/10.18632/aging.103275 pp 10506—10516

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Zhao Y, Yin H, Zhang X, . Modification of graphene oxide by angiopep-2 enhances anti-glioma efficiency of the nanoscaled delivery system for doxorubicin. . 12:10506-10516. https://doi.org/10.18632/aging.103275

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                TY  - JOUR
                AU  - Zhao, Yue 
                AU  - Yin, Hang 
                AU  - Zhang, Xiaoyu 
                TI  - Modification of graphene oxide by angiopep-2 enhances anti-glioma efficiency of the nanoscaled delivery system for doxorubicin
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103275
                DO  - 10.18632/aging.103275
                SP  - 10506
                EP  - 10516
                PY  - 
                AB  - Objective: This study aimed to evaluate the efficacy of the improved nanoscaled delivery system for doxorubicin (Dox) based on angiopep (ANG)-2 modified graphene oxide (GO), the so-called ANG-Dox-GO, in suppressing the growth and and metastasis of glioma cells.Results: Modification of GO by angiopep-2 significantly increased the cellular uptake of Dox. In addition, ANG-Dox-GO treatment of U87 MG cells significantly inhibited cell viability, decreased clone number, cell migration and invasion andinduced cell apoptosis, with superior efficiency over that of Dox-GO and free Dox. Similar results were observed in in vivo experiments&#x2014;tumor size and weight of glioma xenograft mice were obviously decreased after treatments with ANG-Dox-GO, Dox-GO and Dox, respectively, as compared with control group, and the efficiency was the highest in ANG-Dox-GO, followed by Dox-Go and Dox.Conclusions: ANG-Dox-GO exhibited superior anti-glioma effects over Dox-GO both in vitro and in vivo experiments.Methods: The morphology of ANG-Dox-GO was analyzed by UV visible absorption spectroscopy and atomic force microscopy and its in vitro cellular uptake was measured using confocal imaging analysis. The antitumor effects of GO, unbound Dox, Dox-GO and ANG-Dox-GO were evaluated by MTT assay, colony-forming assay, cell apoptosis assay and Transwell assay in U87 malignant glioma (MG) cells.
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LncRNA SOCS2-AS1 inhibits progression and metastasis of colorectal cancer through stabilizing SOCS2 and sponging miR-1264

Zhihai Zheng, Xiaoxiao Li, Heyi You, Xiaofeng Zheng, Xiaojiao Ruan,

https://doi.org/10.18632/aging.103276 pp 10517—10526

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Zheng Z, Li X, You H, Zheng X, Ruan X, . LncRNA SOCS2-AS1 inhibits progression and metastasis of colorectal cancer through stabilizing SOCS2 and sponging miR-1264. . 12:10517-10526. https://doi.org/10.18632/aging.103276

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                TY  - JOUR
                AU  - Zheng, Zhihai 
                AU  - Li, Xiaoxiao 
                AU  - You, Heyi 
                AU  - Zheng, Xiaofeng 
                AU  - Ruan, Xiaojiao 
                TI  - LncRNA SOCS2-AS1 inhibits progression and metastasis of colorectal cancer through stabilizing SOCS2 and sponging miR-1264
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103276
                DO  - 10.18632/aging.103276
                SP  - 10517
                EP  - 10526
                PY  - 
                AB  - Abnormal expression of long noncoding RNA (lncRNA) is involved in human cancers, including colorectal cancer (CRC). However, their functional mechanism is largely unknown. In this study, we explored the roles of lncRNA SOCS2-AS1 in modulating CRC progression. We showed that SOCS2-AS1 was lowly expressed in CRC tissues and cells. SOCS2-AS1 downregulation predicted a poor prognosis in patients with CRC. SOCS2-AS1 overexpression significantly suppressed CRC cell proliferation, colony formation, EdU incorporation, cell-cycle, migration and invasion in vitro while SOCS2-AS1 knockdown led to an opposite phenotype. SOCS2-AS1 overexpression inhibited CRC growth and metastasis in vivo. Mechanistically, we discovered that SOCS2-AS1 was positively correlated with SOCS2 expression in CRC tissues. SOCS2-AS1 contributes to SOCS2 expression through restraining miR-1264. Additionally, we showed that SOCS2 silencing abrogated the suppressive effects of SOCS2-AS1 overexpression. Taken together, our results identified a novel regulatory loop in which SOCS2-AS1/miR-1264/SOCS2 axis suppresses CRC progression.
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Human amnion-derived mesenchymal stem cells promote osteogenic differentiation of human bone marrow mesenchymal stem cells via H19/miR-675/APC axis

Xiaojie Ma, Yifeng Bian, Hua Yuan, Ning Chen, Yongchu Pan, Weina Zhou, Shiyu Gao, Xin Du, Shushu Hao, Zixin Yan, Xuan Li, Keyue Liu, Fan Xu, Yuli Wang, Yifei Du,

https://doi.org/10.18632/aging.103277 pp 10527—10543

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Ma X, Bian Y, Yuan H, Chen N, Pan Y, Zhou W, Gao S, Du X, Hao S, Yan Z, Li X, Liu K, Xu F, et al, . Human amnion-derived mesenchymal stem cells promote osteogenic differentiation of human bone marrow mesenchymal stem cells via H19/miR-675/APC axis. . 12:10527-10543. https://doi.org/10.18632/aging.103277

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                TY  - JOUR
                AU  - Ma, Xiaojie 
                AU  - Bian, Yifeng 
                AU  - Yuan, Hua 
                AU  - Chen, Ning 
                AU  - Pan, Yongchu 
                AU  - Zhou, Weina 
                AU  - Gao, Shiyu 
                AU  - Du, Xin 
                AU  - Hao, Shushu 
                AU  - Yan, Zixin 
                AU  - Li, Xuan 
                AU  - Liu, Keyue 
                AU  - Xu, Fan 
                AU  - Wang, Yuli 
                AU  - Du, Yifei 
                TI  - Human amnion-derived mesenchymal stem cells promote osteogenic differentiation of human bone marrow mesenchymal stem cells via H19/miR-675/APC axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103277
                DO  - 10.18632/aging.103277
                SP  - 10527
                EP  - 10543
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Ma, Xiaojie 
                AU  - Bian, Yifeng 
                AU  - Yuan, Hua 
                AU  - Chen, Ning 
                AU  - Pan, Yongchu 
                AU  - Zhou, Weina 
                AU  - Gao, Shiyu 
                AU  - Du, Xin 
                AU  - Hao, Shushu 
                AU  - Yan, Zixin 
                AU  - Li, Xuan 
                AU  - Liu, Keyue 
                AU  - Xu, Fan 
                AU  - Wang, Yuli 
                AU  - Du, Yifei 
                TI  - Human amnion-derived mesenchymal stem cells promote osteogenic differentiation of human bone marrow mesenchymal stem cells via H19/miR-675/APC axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103277
                DO  - 10.18632/aging.103277
                SP  - 10527
                EP  - 10543
                PY  - 
                AB  - Bone volume inadequacy is an emerging clinical problem impairing the feasibility and longevity of dental implants. Human bone marrow mesenchymal stem cells (HBMSCs) have been widely used in bone remodeling and regeneration. This study examined the effect of long noncoding RNAs (lncRNAs)-H19 on the human amnion-derived mesenchymal stem cells (HAMSCs)-droved osteogenesis in HBMSCs. HAMSCs and HBMSCs were isolated from abandoned amniotic membrane samples and bone marrow. The coculture system was conducted using transwells, and H19 level was measured by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR). The mechanism was further verified. We here discovered that osteogenesis of HBMSCs was induced by HAMSCs, while H19 level in HAMSCs was increased during coculturing. H19 had no significant effect on the proliferative behaviors of HBMSCs, while its overexpression of H19 in HAMSCs led to the upregulated osteogenesis of HBMSCs in vivo and in vitro; whereas its knockdown reversed these effects. Mechanistically, H19 promoted miR-675 expression and contributed to the competitively bounding of miR-675 and Adenomatous polyposis coli (APC), thus significantly activating the Wnt/&#x3B2;-catenin pathway. The results suggested that HAMSCs promote osteogenic differentiation of HBMSCs via H19/miR-675/APC pathway, and supply a potential target for the therapeutic treatment of bone-destructive diseases.
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Long noncoding RNA LINC00460 conduces to tumor growth and metastasis of hepatocellular carcinoma through miR-342-3p-dependent AGR2 up-regulation

Han Hong, Chengjun Sui, Tao Qian, Xiaoyong Xu, Xiang Zhu, Qiang Fei, Jiamei Yang, Minhui Xu,

https://doi.org/10.18632/aging.103278 pp 10544—10555

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Hong H, Sui C, Qian T, Xu X, Zhu X, Fei Q, Yang J, Xu M, . Long noncoding RNA LINC00460 conduces to tumor growth and metastasis of hepatocellular carcinoma through miR-342-3p-dependent AGR2 up-regulation. . 12:10544-10555. https://doi.org/10.18632/aging.103278

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                TY  - JOUR
                AU  - Hong, Han 
                AU  - Sui, Chengjun 
                AU  - Qian, Tao 
                AU  - Xu, Xiaoyong 
                AU  - Zhu, Xiang 
                AU  - Fei, Qiang 
                AU  - Yang, Jiamei 
                AU  - Xu, Minhui 
                TI  - Long noncoding RNA LINC00460 conduces to tumor growth and metastasis of hepatocellular carcinoma through miR-342-3p-dependent AGR2 up-regulation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103278
                DO  - 10.18632/aging.103278
                SP  - 10544
                EP  - 10555
                PY  - 
                AB  - Hepatocellular carcinoma (HCC) is the fifth most common malignant tumor in the world. It ranks third among cancer-induced deaths worldwide and has the characteristics of high metastasis and high recurrence rate. Long non-coding RNA (LncRNA) LINC00460 is significantly up-regulated in multiple types of cancers and is closely related to the progression of tumors. However, effects of LINC00460 and corresponding regulatory path in HCC are still poorly investigated.In our study, we found that expression of LINC00460 was up-regulated in HCC tissues and cell lines compared with the control. Then we revealed that knockdown of LINC00460 suppressed cell proliferation and cell mobility and induced cell apoptosis in HCC cells. Further study demonstrated that knockdown of LINC00460 suppressed the progression of HCC by elevating the expression of microRNA (miRNA, miR)-342-3p. Besides that, metastasis marker, Anterior gradient homolog 2 (AGR2) was found to be a target of miR-342-3p and overexpression of AGR2 promoted the progression of HCC. Finally, the in vivo experiments further verified the anti-tumor effects of LINC00460 / miR-342-3p / AGR2 axis in HCC.The LINC00460 / miR-342-3p / AGR2 axis exerts anti-tumor effect in HCC in vitro and in vivo, consolidating and expanding the research about targeted gene therapy for early diagnosis and treatment of HCC.
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T1-11, an adenosine derivative, ameliorates aging-related behavioral physiology and senescence markers in aging mice

Wei-Hsiang Hsu, Young-Ji Shiao, Yen-Ming Chao, Yi-Jeng Huang, Yun-Lian Lin,

https://doi.org/10.18632/aging.103279 pp 10556—10577

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Hsu W, Shiao Y, Chao Y, Huang Y, Lin Y, . T1-11, an adenosine derivative, ameliorates aging-related behavioral physiology and senescence markers in aging mice. . 12:10556-10577. https://doi.org/10.18632/aging.103279

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                TY  - JOUR
                AU  - Hsu, Wei-Hsiang 
                AU  - Shiao, Young-Ji 
                AU  - Chao, Yen-Ming 
                AU  - Huang, Yi-Jeng 
                AU  - Lin, Yun-Lian 
                TI  - T1-11, an adenosine derivative, ameliorates aging-related behavioral physiology and senescence markers in aging mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103279
                DO  - 10.18632/aging.103279
                SP  - 10556
                EP  - 10577
                PY  - 
                AB  - Aging is a natural human process. It is uniquely individual, taking into account experiences, lifestyle habits and environmental factors. However, many disorders and syndromes, such as osteoporosis, neurodegenerative disorders, cognitive decline etc., often come with aging. The present study was designed to investigate the possible anti-aging effect of N6-(4-hydroxybenzyl)adenine riboside (T1-11), an adenosine analog isolated from Gastrodia elata, in a mouse model of aging created by D-galactose (D-gal) and the underlying mechanism, as well as explore the role of adenosine signaling in aging. T1-11 activated A2AR and suppressed D-gal- and BeSO4-induced cellular senescence in vitro. In vivo results in mice revealed that T1-11 abated D-gal-induced reactive oxygen species generation and ameliorated cognitive decline by inducing neurogenesis and lowering D-gal-caused neuron death. T1-11 could be a potent agent for postponing senility and preventing aging-related neuroinflammation and neurodegeneration.
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CARM1 promotes non-small cell lung cancer progression through upregulating CCNE2 expression

Deqin Wu, Jing He, Wei Zhang, Kai Wang, Shidai Jin, Jun Li, Wen Gao,

https://doi.org/10.18632/aging.103280 pp 10578—10593

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Wu D, He J, Zhang W, Wang K, Jin S, Li J, Gao W, . CARM1 promotes non-small cell lung cancer progression through upregulating CCNE2 expression. . 12:10578-10593. https://doi.org/10.18632/aging.103280

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                TY  - JOUR
                AU  - Wu, Deqin 
                AU  - He, Jing 
                AU  - Zhang, Wei 
                AU  - Wang, Kai 
                AU  - Jin, Shidai 
                AU  - Li, Jun 
                AU  - Gao, Wen 
                TI  - CARM1 promotes non-small cell lung cancer progression through upregulating CCNE2 expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103280
                DO  - 10.18632/aging.103280
                SP  - 10578
                EP  - 10593
                PY  - 
                AB  - The underlying molecular mechanisms of tumorigenesis and progression of non-small cell lung cancer (NSCLC) are not yet fully elucidated. In the present study, in vitro functional dissections suggest that siRNA-mediated silencing of CCNE2 profoundly attenuated the proliferative and colony-formative abilities of NSCLC PC9 and HCC827 cells, while forced overexpression of CCNE2 significantly strengthened the proliferative and colony-formative capabilities of these cells. Intriguingly, by ChIP and luciferase reporter gene assays, we observed that CARM1 is recruited to the promoter regions of CCNE2 gene and acts as a transcriptional activator. Mechanically, the asymmetric di-methylation of H3R17me2a and H3R26me2a, as the catalytic substrates of CARM1, were highly enriched at the core promoter regions of CCNE2 gene, thereby activating the expression of CCNE2. In vitro and in vivo rescue experiments demonstrated that restoration of CCNE2 expression significantly abolished the CARM1 shRNA-mediated inhibition of cell proliferation, indicating that the oncogenic function of CARM1, at least partially, depended on the activation of CCNE2. Inhibition of CARM1 enzymatic activity could significantly repress CCNE2 expression in NSCLC cells. In addition, the expression of CARM1 was significantly elevated and positively correlated with CCNE2 levels in 20 cases of NSCLC patients. Both CARM1 and CCNE2 are highly associated with shorter 10-year overall survival of at a large cohort of 461 cases of NSCLC patients from the Kaplan-Meier plotter database. To summarize, these findings provide compelling evidence that CARM1 could promote NSCLC progression via activation of CCNE2, paving the way for future therapeutic strategies in NSCLC.
                ER  -

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Coagulation factor 2 thrombin receptor promotes malignancy in glioma under SOX2 regulation

Guojun Gao, Ming Yang, Fan Wang, Ge Dang, Xiaoling Zhang, Jing Zhao, Xiangyang Wang, Baozhe Jin,

https://doi.org/10.18632/aging.103281 pp 10594—10613

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Gao G, Yang M, Wang F, Dang G, Zhang X, Zhao J, Wang X, Jin B, . Coagulation factor 2 thrombin receptor promotes malignancy in glioma under SOX2 regulation. . 12:10594-10613. https://doi.org/10.18632/aging.103281

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                TY  - JOUR
                AU  - Gao, Guojun 
                AU  - Yang, Ming 
                AU  - Wang, Fan 
                AU  - Dang, Ge 
                AU  - Zhang, Xiaoling 
                AU  - Zhao, Jing 
                AU  - Wang, Xiangyang 
                AU  - Jin, Baozhe 
                TI  - Coagulation factor 2 thrombin receptor promotes malignancy in glioma under SOX2 regulation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103281
                DO  - 10.18632/aging.103281
                SP  - 10594
                EP  - 10613
                PY  - 
                AB  - Glioma is the most common human primary brain cancer with high mortality and unfavorable clinical outcome. Coagulation factor 2 thrombin receptor (F2R), is a key component in the thrombosis process and has been demonstrated upregulated in various cancers. However, the effect and molecular mechanisms of F2R in glioma remains unclear. In our study, we confirmed that the expression of F2R was upregulated in glioma and predicted poor prognosis. Gene Set Enrichment Analysis (GSEA) and function assays demonstrated that F2R overexpression promoted glioma cell proliferation, metastasis and epithelial-mesenchymal transition (EMT) in vitro and tumor growth in vivo. Then, we identified and validated F2R was the target gene of SRY-box 2 (SOX2) by dual luciferase reporter assay and chromatin immunoprecipitation assay. Besides, High expression of F2R in malignant glioma was associated with &#x3B2;-catenint signaling pathway activation. Our findings conclude that F2R promotes glioma cell proliferation and metastasis under SOX2 and actives WNT/&#x3B2;-catenin Signaling pathway, which provides novel insight to the therapeutic regimen in glioma.
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Ursolic acid reverses liver fibrosis by inhibiting interactive NOX4/ROS and RhoA/ROCK1 signalling pathways

Sizhe Wan, Fangyun Luo, Chenkai Huang, Cong Liu, Qingtian Luo, Xuan Zhu,

https://doi.org/10.18632/aging.103282 pp 10614—10632

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Wan S, Luo F, Huang C, Liu C, Luo Q, Zhu X, . Ursolic acid reverses liver fibrosis by inhibiting interactive NOX4/ROS and RhoA/ROCK1 signalling pathways. . 12:10614-10632. https://doi.org/10.18632/aging.103282

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                TY  - JOUR
                AU  - Wan, Sizhe 
                AU  - Luo, Fangyun 
                AU  - Huang, Chenkai 
                AU  - Liu, Cong 
                AU  - Luo, Qingtian 
                AU  - Zhu, Xuan 
                TI  - Ursolic acid reverses liver fibrosis by inhibiting interactive NOX4/ROS and RhoA/ROCK1 signalling pathways
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103282
                DO  - 10.18632/aging.103282
                SP  - 10614
                EP  - 10632
                PY  - 
                AB  - Liver fibrosis is the reversible deposition of extracellular matrix (ECM) and scar formation after liver damage by various stimuli. The interaction between NOX4/ROS and RhoA/ROCK1 in liver fibrosis is not yet clear. Ursolic acid (UA) is a traditional Chinese medicine with anti-fibrotic effects, but the molecular mechanism underlying these effects is still unclear. We investigated the interaction between NOX4/ROS and RhoA/ROCK1 during liver fibrosis and whether these molecules are targets for the anti-fibrotic effects of UA. First, we confirmed that UA reversed CCl4-induced liver fibrosis. In the NOX4 intervention and RhoA intervention groups, related experimental analyses confirmed the decrease in CCl4-induced liver fibrosis. Next, we determined that the expression of NOX4 and RhoA/ROCK1 was decreased in UA-treated liver fibrotic mice. Furthermore, RhoA/ROCK1 expression was decreased in the NOX4 intervention group, but there was no significant change in the expression of NOX4 in the RhoA intervention group. Finally, we found that liver fibrotic mice showed a decline in their microbiota diversity and abundance, a change in their microbiota composition, and a reduction in the number of potential beneficial bacteria. However, in UA-treated liver fibrotic mice, the microbiota dysbiosis was ameliorated. In conclusion, the NOX4/ROS and RhoA/ROCK1 signalling pathways are closely linked to the development of liver fibrosis. UA can reverse liver fibrosis by inhibiting the NOX4/ROS and RhoA/ROCK1 signalling pathways, which may interact with each other.
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Gut microbiota–dependent Trimethylamine N-Oxide are related with hip fracture in postmenopausal women: a matched case-control study

Yakun Liu, Yan-Long Guo, Shan Meng, Hua Gao, Li-Juan Sui, Shaobin Jin, Yang Li, Shao-Guang Fan,

https://doi.org/10.18632/aging.103283 pp 10633—10641

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Liu Y, Guo Y, Meng S, Gao H, Sui L, Jin S, Li Y, Fan S, . Gut microbiota–dependent Trimethylamine N-Oxide are related with hip fracture in postmenopausal women: a matched case-control study. . 12:10633-10641. https://doi.org/10.18632/aging.103283

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                TY  - JOUR
                AU  - Liu, Yakun 
                AU  - Guo, Yan-Long 
                AU  - Meng, Shan 
                AU  - Gao, Hua 
                AU  - Sui, Li-Juan 
                AU  - Jin, Shaobin 
                AU  - Li, Yang 
                AU  - Fan, Shao-Guang 
                TI  - Gut microbiota–dependent Trimethylamine N-Oxide are related with hip fracture in postmenopausal women: a matched case-control study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103283
                DO  - 10.18632/aging.103283
                SP  - 10633
                EP  - 10641
                PY  - 
                AB  - The study evaluates the serum levels of Trimethylamine N-Oxide (TMAO), a gut microbial metabolite, in 286 postmenopausal women with hip fracture. From January 1, 2018 to December 31, 2018, eligible patients were included. Same women without fracture mated age were enrolled. TMAO serum levels were tested by ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). The serum levels of TMAO were significantly higher in patients with hip fracture than in those controls (P&lt;0.001). The serum levels of TMAO were also higher in patients with hip fracture only than in those who also had upper limb fracture (P=0.001). High level of TMAO was proved a predictor of both hip fracture and had upper limb fracture combined hip fracture, after the adjustment of other existing risk factors [e.g., for each 1 uM increase of TMAO, odd ratio 1.16 (95% CI, 1.07&#x2013;1.25), P &lt; 0.001; and 1.12 (95% CI, 1.03&#x2013;1.26), P=0.008, respectively]. In summary, increased TMAO serum levels associated with high risk of hip fracture, suggesting that increase TMAO may contribute to osteoporosis and fracture in postmenopausal women.
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Epigenome-wide gene–age interaction analysis reveals reversed effects of PRODH DNA methylation on survival between young and elderly early-stage NSCLC patients

Chao Chen, Yongyue Wei, Liangmin Wei, Jiajin Chen, Xin Chen, Xuesi Dong, Jieyu He, Lijuan Lin, Ying Zhu, Hui Huang, Dongfang You, Linjing Lai, Sipeng Shen, Weiwei Duan, Li Su, Andrea Shafer, Thomas Fleischer, Maria Moksnes Bjaanæs, Anna Karlsson, Maria Planck, Rui Wang, Johan Staaf, Åslaug Helland, Manel Esteller, Ruyang Zhang, Feng Chen, David C. Christiani,

https://doi.org/10.18632/aging.103284 pp 10642—10662

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Chen C, Wei Y, Wei L, Chen J, Chen X, Dong X, He J, Lin L, Zhu Y, Huang H, You D, Lai L, Shen S, et al, . Epigenome-wide gene–age interaction analysis reveals reversed effects of PRODH DNA methylation on survival between young and elderly early-stage NSCLC patients. . 12:10642-10662. https://doi.org/10.18632/aging.103284

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Provider: 
 TY - JOUR
 AU - Chen, Chao 
 AU - Wei, Yongyue 
 AU - Wei, Liangmin 
 AU - Chen, Jiajin 
 AU - Chen, Xin 
 AU - Dong, Xuesi 
 AU - He, Jieyu 
 AU - Lin, Lijuan 
 AU - Zhu, Ying 
 AU - Huang, Hui 
 AU - You, Dongfang 
 AU - Lai, Linjing 
 AU - Shen, Sipeng 
 AU - Duan, Weiwei 
 AU - Su, Li 
 AU - Shafer, Andrea 
 AU - Fleischer, Thomas 
 AU - Bjaanæs, Maria Moksnes 
 AU - Karlsson, Anna 
 AU - Planck, Maria 
 AU - Wang, Rui 
 AU - Staaf, Johan 
 AU - Helland, Åslaug 
 AU - Esteller, Manel 
 AU - Zhang, Ruyang 
 AU - Chen, Feng 
 AU - Christiani, David C. 
 TI - Epigenome-wide gene–age interaction analysis reveals reversed effects of PRODH DNA methylation on survival between young and elderly early-stage NSCLC patients
 JO - 
 JA - 
 VL - 12
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103284
 DO - 10.18632/aging.103284
 SP - 10642
 EP - 10662
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Chen, Chao 
 AU - Wei, Yongyue 
 AU - Wei, Liangmin 
 AU - Chen, Jiajin 
 AU - Chen, Xin 
 AU - Dong, Xuesi 
 AU - He, Jieyu 
 AU - Lin, Lijuan 
 AU - Zhu, Ying 
 AU - Huang, Hui 
 AU - You, Dongfang 
 AU - Lai, Linjing 
 AU - Shen, Sipeng 
 AU - Duan, Weiwei 
 AU - Su, Li 
 AU - Shafer, Andrea 
 AU - Fleischer, Thomas 
 AU - Bjaanæs, Maria Moksnes 
 AU - Karlsson, Anna 
 AU - Planck, Maria 
 AU - Wang, Rui 
 AU - Staaf, Johan 
 AU - Helland, Åslaug 
 AU - Esteller, Manel 
 AU - Zhang, Ruyang 
 AU - Chen, Feng 
 AU - Christiani, David C. 
 TI - Epigenome-wide gene–age interaction analysis reveals reversed effects of PRODH DNA methylation on survival between young and elderly early-stage NSCLC patients
 JO - 
 JA - 
 VL - 12
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103284
 DO - 10.18632/aging.103284
 SP - 10642
 EP - 10662
 PY - 
 AB - DNA methylation changes during aging, but it remains unclear whether the effect of DNA methylation on lung cancer survival varies with age. Such an effect could decrease prediction accuracy and treatment efficacy. We performed a methylation&#x2013;age interaction analysis using 1,230 early-stage lung adenocarcinoma patients from five cohorts. A Cox proportional hazards model was used to investigate lung adenocarcinoma and squamous cell carcinoma patients for methylation&#x2013;age interactions, which were further confirmed in a validation phase. We identified one adenocarcinoma-specific CpG probe, cg14326354PRODH, with effects significantly modified by age (HRinteraction = 0.989; 95% CI: 0.986&#x2013;0.994; P = 9.18&#xD7;10&#x2013;7). The effect of low methylation was reversed for young and elderly patients categorized by the boundary of 95% CI standard (HRyoung = 2.44; 95% CI: 1.26&#x2013;4.72; P = 8.34&#xD7;10-3; HRelderly = 0.58; 95% CI: 0.42&#x2013;0.82; P = 1.67&#xD7;10-3). Moreover, there was an antagonistic interaction between low cg14326354PRODH methylation and elderly age (HRinteraction = 0.21; 95% CI: 0.11&#x2013;0.40; P = 2.20&#xD7;10&#x2212;6). In summary, low methylation of cg14326354PRODH might benefit survival of elderly lung adenocarcinoma patients, providing new insight to age-specific prediction and potential drug targeting.
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Association between immune-related adverse events and efficacy of PD-1 inhibitors in Chinese patients with advanced melanoma

Jing-Jing Zhao, Xi-Zhi Wen, Ya Ding, Dan-Dan Li, Bao-Yan Zhu, Jing-Jing Li, De-Sheng Weng, Xing Zhang, Xiao-Shi Zhang,

https://doi.org/10.18632/aging.103285 pp 10663—10675

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Zhao J, Wen X, Ding Y, Li D, Zhu B, Li J, Weng D, Zhang X, Zhang X, . Association between immune-related adverse events and efficacy of PD-1 inhibitors in Chinese patients with advanced melanoma. . 12:10663-10675. https://doi.org/10.18632/aging.103285

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                TY  - JOUR
                AU  - Zhao, Jing-Jing 
                AU  - Wen, Xi-Zhi 
                AU  - Ding, Ya 
                AU  - Li, Dan-Dan 
                AU  - Zhu, Bao-Yan 
                AU  - Li, Jing-Jing 
                AU  - Weng, De-Sheng 
                AU  - Zhang, Xing 
                AU  - Zhang, Xiao-Shi 
                TI  - Association between immune-related adverse events and efficacy of PD-1 inhibitors in Chinese patients with advanced melanoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103285
                DO  - 10.18632/aging.103285
                SP  - 10663
                EP  - 10675
                PY  - 
                AB  - Programmed cell death 1 (PD-1) checkpoint inhibitor therapy leads to immune-related adverse events (irAEs). We sought to evaluate whether the development of irAEs correlates with the treatment response in Chinese patients with advanced melanoma. In this study, we conducted a retrospective study of advanced melanoma patients who received PD-1 inhibitor therapy in China between August 2014 and March 2018. A total of 93 patients treated with PD-1 inhibitors including pembrolizumab and nivolumab were enrolled. The most frequent irAEs were pruritus, rash, vitiligo, and fatigue. The median time to onset of irAEs was 6.1 weeks. The overall response rate (ORR) and disease control rate (DCR) were higher in patients with irAEs than those without irAEs (P = 0.004 and P = 0.003, respectively), and better in patients who experienced three or more irAEs than those with none (P &lt;0.001 and P &lt;0.001, respectively). The ORR and DCR were significantly better in patients with grade 1 to 2 irAEs when compared with those with none (P = 0.002 and P = 0.003, respectively). In addition, the median progression-free survival and overall survival were longer in patients with irAEs than in those without irAEs (P = 0.007 and P = 0.002, respectively). In conclusion, our data demonstrated that irAEs were associated with a better clinical outcome after treatment with PD-1 inhibitor therapy in Chinese patients with advanced melanoma.
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Modelling biological age based on plasma peptides in Han Chinese adults

Weijie Cao, Deqiang Zheng, Guohua Wang, Jie Zhang, Siqi Ge, Manjot Singh, Hao Wang, Manshu Song, Dong Li, Wei Wang, Xizhu Xu, Youxin Wang,

https://doi.org/10.18632/aging.103286 pp 10676—10686

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Cao W, Zheng D, Wang G, Zhang J, Ge S, Singh M, Wang H, Song M, Li D, Wang W, Xu X, Wang Y, . Modelling biological age based on plasma peptides in Han Chinese adults. . 12:10676-10686. https://doi.org/10.18632/aging.103286

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                TY  - JOUR
                AU  - Cao, Weijie 
                AU  - Zheng, Deqiang 
                AU  - Wang, Guohua 
                AU  - Zhang, Jie 
                AU  - Ge, Siqi 
                AU  - Singh, Manjot 
                AU  - Wang, Hao 
                AU  - Song, Manshu 
                AU  - Li, Dong 
                AU  - Wang, Wei 
                AU  - Xu, Xizhu 
                AU  - Wang, Youxin 
                TI  - Modelling biological age based on plasma peptides in Han Chinese adults
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103286
                DO  - 10.18632/aging.103286
                SP  - 10676
                EP  - 10686
                PY  - 
                AB  - Age-related disease burdens increased over time, and whether plasma peptides can be used to accurately predict age in order to explain the variation in biological indicators remains inadequately understood. Here we first developed a biological age model based on plasma peptides in 1890 Chinese Han adults. Based on mass spectrometry, 84 peptides were detected with masses in the range of 0.6-10.0 kDa, and 13 of these peptides were identified as known amino acid sequences. Five of these thirteen plasma peptides, including fragments of apolipoprotein A-I (m/z 2883.99), fibrinogen alpha chain (m/z 3060.13), complement C3 (m/z 2190.59), complement C4-A (m/z 1898.21), and breast cancer type 2 susceptibility protein (m/z 1607.84) were finally included in the final model by performing a multivariate linear regression with stepwise selection. This biological age model accounted for 72.3% of the variation in chronological age. Furthermore, the linear correlation between the actual age and biological age was 0.851 (95% confidence interval: 0.836-0.864) and 0.842 (95% confidence interval: 0.810-0.869) in the training and validation sets, respectively. The biological age based on plasma peptides has potential positive effects on primary prevention, and its biological meaning warrants further investigation.
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Leisure activities and disability in activities of daily living among the oldest-old Chinese population: evidence from the Chinese Longitudinal Healthy Longevity Study

Zhi-Hao Li, Qing Chen, Virginia Byers Kraus, Dong Shen, Xi-Ru Zhang, Pei-Dong Zhang, Wen-Fang Zhong, Yue-Bin Lv, Qing-Mei Huang, Wei-Qi Song, Dong Wang, Xian-Bo Wu, Xiao-Ming Shi, Chen Mao,

https://doi.org/10.18632/aging.103287 pp 10687—10703

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Li Z, Chen Q, Byers Kraus V, Shen D, Zhang X, Zhang P, Zhong W, Lv Y, Huang Q, Song W, Wang D, Wu X, Shi X, et al, . Leisure activities and disability in activities of daily living among the oldest-old Chinese population: evidence from the Chinese Longitudinal Healthy Longevity Study. . 12:10687-10703. https://doi.org/10.18632/aging.103287

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                TY  - JOUR
                AU  - Li, Zhi-Hao 
                AU  - Chen, Qing 
                AU  - Byers Kraus, Virginia 
                AU  - Shen, Dong 
                AU  - Zhang, Xi-Ru 
                AU  - Zhang, Pei-Dong 
                AU  - Zhong, Wen-Fang 
                AU  - Lv, Yue-Bin 
                AU  - Huang, Qing-Mei 
                AU  - Song, Wei-Qi 
                AU  - Wang, Dong 
                AU  - Wu, Xian-Bo 
                AU  - Shi, Xiao-Ming 
                AU  - Mao, Chen 
                TI  - Leisure activities and disability in activities of daily living among the oldest-old Chinese population: evidence from the Chinese Longitudinal Healthy Longevity Study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103287
                DO  - 10.18632/aging.103287
                SP  - 10687
                EP  - 10703
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Li, Zhi-Hao 
                AU  - Chen, Qing 
                AU  - Byers Kraus, Virginia 
                AU  - Shen, Dong 
                AU  - Zhang, Xi-Ru 
                AU  - Zhang, Pei-Dong 
                AU  - Zhong, Wen-Fang 
                AU  - Lv, Yue-Bin 
                AU  - Huang, Qing-Mei 
                AU  - Song, Wei-Qi 
                AU  - Wang, Dong 
                AU  - Wu, Xian-Bo 
                AU  - Shi, Xiao-Ming 
                AU  - Mao, Chen 
                TI  - Leisure activities and disability in activities of daily living among the oldest-old Chinese population: evidence from the Chinese Longitudinal Healthy Longevity Study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103287
                DO  - 10.18632/aging.103287
                SP  - 10687
                EP  - 10703
                PY  - 
                AB  - Introduction: To investigate the independent and joint effects of leisure activities on disability in activities of daily living (ADL) among the oldest-old Chinese population (aged &#x2265; 80 years).Results: A total of 3696 participants with ADL disability were identified during the median follow-up period of 3.1 years. Compared to the participants who &#x201C;never&#x201D; watched TV or listened to the radio and who &#x201C;never&#x201D; kept domestic animals or pets, those who engaged in these activities &#x201C;almost every day&#x201D; had a significantly lower ADL disability risk (adjusted hazard ratios were 0.74 and 0.66, respectively; both P &lt; 0.001). Furthermore, participants engaging in multiple leisure activities showed a reduced risk of ADL disability (P for trend &lt; 0.001).Conclusions: Frequently watching TV or listening to the radio and keeping domestic animals or pets was associated with a lower risk of ADL disability among the oldest-old Chinese population.Methods: We included 12,331 participants (aged &#x2265; 80 years) (mean [SD] age: 89.5 [7.0] years) who managed to perform ADL independently at baseline in the Chinese Longitudinal Healthy Longevity Survey 1998-2014 waves. Cox proportional hazards models were used to examine whether leisure activities were associated with ADL disability.
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Walking ability and functional status after post-acute care for stroke rehabilitation in different age groups: a prospective study based on propensity score matching

Chung-Yuan Wang, Seido Miyoshi, Chang-Hung Chen, Kai-Chun Lee, Long-Chung Chang, Jo-Hsuan Chung, Hon-Yi Shi,

https://doi.org/10.18632/aging.103288 pp 10704—10714

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Wang C, Miyoshi S, Chen C, Lee K, Chang L, Chung J, Shi H, . Walking ability and functional status after post-acute care for stroke rehabilitation in different age groups: a prospective study based on propensity score matching. . 12:10704-10714. https://doi.org/10.18632/aging.103288

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                TY  - JOUR
                AU  - Wang, Chung-Yuan 
                AU  - Miyoshi, Seido 
                AU  - Chen, Chang-Hung 
                AU  - Lee, Kai-Chun 
                AU  - Chang, Long-Chung 
                AU  - Chung, Jo-Hsuan 
                AU  - Shi, Hon-Yi 
                TI  - Walking ability and functional status after post-acute care for stroke rehabilitation in different age groups: a prospective study based on propensity score matching
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103288
                DO  - 10.18632/aging.103288
                SP  - 10704
                EP  - 10714
                PY  - 
                AB  - Few studies have compared how rehabilitative post-acute care affects recovery of walking ability and other functions after stroke in different age groups. After propensity score matching (1:1), 316 stroke patients were separated into an aged group (age &#x2265;65 years, n=158) and a non-aged group (age &lt;65 years, n=158). Both groups significantly improved in Barthel index, EuroQol-5 dimension, Berg balance scale, 6-minute walking distance and 5-meter walking speed (P&lt;0.001). The non-aged group had significantly larger improvements in Berg balance scale, instrumental activities of daily living, EuroQol-5 dimension and 6-minute walking distance (P&lt;0.001) compared to the aged group. The two groups did not significantly differ in Barthel index, 5-meter walking speed, length of stay, and cost. The aged group had poorer walking ability and poorer instrumental activities of daily living compared to the non-aged group. After intensive rehabilitative post-acute care, however, the aged group improved in walking ability, functional performance and mental health. Intensive strength training for unaffected lower limbs in the stroke patients achieved good recovery of walking ability and other functions. Overall, intensive rehabilitative post-acute care improved self-care ability and decreased informal care costs. Rehabilitative PAC under per-diem reimbursement is efficient and economical for stroke patients in an aging society.
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Subgroup analysis of proinsulin and insulin levels reveals novel correlations to metabolic indicators of type 2 diabetes

Tangying Li, Huibiao Quan, Huachuan Zhang, Leweihua Lin, Lu Lin, Qianying Ou, Kaining Chen,

https://doi.org/10.18632/aging.103289 pp 10715—10735

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Li T, Quan H, Zhang H, Lin L, Lin L, Ou Q, Chen K, . Subgroup analysis of proinsulin and insulin levels reveals novel correlations to metabolic indicators of type 2 diabetes. . 12:10715-10735. https://doi.org/10.18632/aging.103289

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                TY  - JOUR
                AU  - Li, Tangying 
                AU  - Quan, Huibiao 
                AU  - Zhang, Huachuan 
                AU  - Lin, Leweihua 
                AU  - Lin, Lu 
                AU  - Ou, Qianying 
                AU  - Chen, Kaining 
                TI  - Subgroup analysis of proinsulin and insulin levels reveals novel correlations to metabolic indicators of type 2 diabetes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103289
                DO  - 10.18632/aging.103289
                SP  - 10715
                EP  - 10735
                PY  - 
                AB  - Proinsulin, insulin and proinsulin/insulin (P/I) ratio have been reported to be correlated with fasting plasma glucose (FPG) and Hemoglobin A1c (HbA1c) in whole population study therefore sensitive predictors of T2D progression. However, by analyzing data collected from 2018-2019 from a cohort of 1579 East Asian individuals from Hainan Province of China, we find that the associations of proinsulin, insulin and P/I ratio with diabetic indicators have distinct, sometimes opposite regression patterns in normal, prediabetic and diabetic subgroups. The strength of the associations are generally weak in normal and prediabetic groups, and only moderate in diabetic group between postprandial proinsulin and HbA1c, between postprandial insulin and FPG or HbA1c, and between postprandial P/I ratio and FPG or HbA1c. Receiver operating characteristic (ROC) curve analysis shows these parameters are weaker than age in predicting diabetes development, with P/I ratio being the weakest. Proinsulin and insulin levels are tightly associated with insulin sensitivity across all subgroups, as measured by Matsuda index. Together, our results suggest that proinsulin, insulin or P/I ratio are weak predictors of diabetes development in the whole population, urging the need for stratifying strategies and novel perspectives in evaluating and predicting hyperglycemia progression.
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Structural and functional changes of gut microbiota in ovariectomized rats and their correlations with altered bone mass

Sicong Ma, Jinhong Qin, Yongqiang Hao, Ying Shi, Lingjie Fu,

https://doi.org/10.18632/aging.103290 pp 10736—10753

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Ma S, Qin J, Hao Y, Shi Y, Fu L, . Structural and functional changes of gut microbiota in ovariectomized rats and their correlations with altered bone mass. . 12:10736-10753. https://doi.org/10.18632/aging.103290

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                TY  - JOUR
                AU  - Ma, Sicong 
                AU  - Qin, Jinhong 
                AU  - Hao, Yongqiang 
                AU  - Shi, Ying 
                AU  - Fu, Lingjie 
                TI  - Structural and functional changes of gut microbiota in ovariectomized rats and their correlations with altered bone mass
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103290
                DO  - 10.18632/aging.103290
                SP  - 10736
                EP  - 10753
                PY  - 
                AB  - As a critical factor involved in the maintenance of physiological homeostasis, the gut microbiota (GM) reportedly plays a key role in bone development. To date, the association between the GM and steroid deficiency-induced osteoporosis remains poorly understood. Forty female Sprague Dawley rats were divided into an ovariectomy (OVX) or control group. We performed 16S rRNA and metagenome sequencing, to compare diversity, taxonomic differences, and functional genes. The GM composition did not change in the control group and the number of operational taxonomic units increased significantly following ovariectomy. Alpha diversity, determined by ACE estimator, CHAO estimator, the Shannon index, and the Simpson index showed an increasing trend after ovariectomy. Samples in the OVX group were well clustered both pre- and post-ovariectomy, as demonstrated by principal coordinate 1 (PC1) and PC2. Functional genes of GM, including those involved in synthesis and metabolism of carbohydrates and nucleotides, microbial structure, and heme, as well as hemin uptake and utilization, increased at the early stage of osteoporosis. We observed that Ruminococcus flavefaciens exhibited the greatest variation in abundance among the GM and this was also associated with osteoclastic indicators and the estrobolome. Specific changes in fecal microbiota are associated with the pathogenesis of steroid deficiency-induced osteoporosis.
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How non-drug interventions affect the quality of life of patients suffering from progressive cognitive decline and their main caregiver

Benedetta Leidi-Maimone, Marie-Laure Notter-Bielser, Marie-Hélène Laouadi, Sarah Perrin, Hélène Métraux, Daniel Damian, Camille F. Chavan, Mélanie Nsir, Gwendoline Cibelli, Marie-Jo Tâche, Marie-Louise Montandon, Joseph Ghika, Jean-François Démonet, Anne-Véronique Dürst, Andrea Brioschi Guevara,

https://doi.org/10.18632/aging.103291 pp 10754—10771

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Leidi-Maimone B, Notter-Bielser M, Laouadi M, Perrin S, Métraux H, Damian D, Chavan CF, Nsir M, Cibelli G, Tâche M, Montandon M, Ghika J, Démonet J, et al, . How non-drug interventions affect the quality of life of patients suffering from progressive cognitive decline and their main caregiver. . 12:10754-10771. https://doi.org/10.18632/aging.103291

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                TY  - JOUR
                AU  - Leidi-Maimone, Benedetta 
                AU  - Notter-Bielser, Marie-Laure 
                AU  - Laouadi, Marie-Hélène 
                AU  - Perrin, Sarah 
                AU  - Métraux, Hélène 
                AU  - Damian, Daniel 
                AU  - Chavan, Camille F. 
                AU  - Nsir, Mélanie 
                AU  - Cibelli, Gwendoline 
                AU  - Tâche, Marie-Jo 
                AU  - Montandon, Marie-Louise 
                AU  - Ghika, Joseph 
                AU  - Démonet, Jean-François 
                AU  - Dürst, Anne-Véronique 
                AU  - Guevara, Andrea Brioschi 
                TI  - How non-drug interventions affect the quality of life of patients suffering from progressive cognitive decline and their main caregiver
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103291
                DO  - 10.18632/aging.103291
                SP  - 10754
                EP  - 10771
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Leidi-Maimone, Benedetta 
                AU  - Notter-Bielser, Marie-Laure 
                AU  - Laouadi, Marie-Hélène 
                AU  - Perrin, Sarah 
                AU  - Métraux, Hélène 
                AU  - Damian, Daniel 
                AU  - Chavan, Camille F. 
                AU  - Nsir, Mélanie 
                AU  - Cibelli, Gwendoline 
                AU  - Tâche, Marie-Jo 
                AU  - Montandon, Marie-Louise 
                AU  - Ghika, Joseph 
                AU  - Démonet, Jean-François 
                AU  - Dürst, Anne-Véronique 
                AU  - Guevara, Andrea Brioschi 
                TI  - How non-drug interventions affect the quality of life of patients suffering from progressive cognitive decline and their main caregiver
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103291
                DO  - 10.18632/aging.103291
                SP  - 10754
                EP  - 10771
                PY  - 
                AB  - Background: In the absence of cure for age-related neurodegenerative diseases, non-drug interventions (NDIs) represent useful options. Quality of life (QOL) is a multidimensional concept progressively affected by cognitive decline. How single or multiple NDIs impact QOL is unknown.Results: We found no significant effect of multiple over single NDI on QOL. Socio-demographic variables influenced patients&#x2019; (age, gender, caregivers&#x2019; occupational status, management of patients&#x2019; financial affairs) and caregivers&#x2019; (gender, occupational status, patients&#x2019; severity of cognitive decline) QOL. When dyads interrupted interventions after 6 months, their QOL was lower and caregivers&#x2019; anxiety, depression and physical symptoms were higher at the end of the study.Conclusions: While the type and number of interventions do not appear to be critical, the continuity of adapted interventions in the long-term might be important for maintaining QOL of patients and caregivers.Methods: This is a multicenter (7 Swiss Memory Clinics), quasi-experimental, one-year follow-up study including 148 subjects (mild cognitive impairment or mild dementia patients and their caregivers). Primary outcome was the effect of multiple vs single NDIs on QOL. Secondary outcome included NDIs effect on patients&#x2019; cognitive impairment and functional autonomy, caregivers&#x2019; burden, severity of patients&#x2019; neuropsychiatric symptoms and dyads&#x2019; anxiety and depression.
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Meta-analysis of the association between nut consumption and the risks of cancer incidence and cancer-specific mortality

Dai Zhang, Cong Dai, Linghui Zhou, Yiche Li, Kang Liu, Yu-Jiao Deng, Na Li, Yi Zheng, Qian Hao, Si Yang, Dingli Song, Ying Wu, Zhen Zhai, Shiyi Cao, Zhijun Dai,

https://doi.org/10.18632/aging.103292 pp 10772—10794

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Zhang D, Dai C, Zhou L, Li Y, Liu K, Deng Y, Li N, Zheng Y, Hao Q, Yang S, Song D, Wu Y, Zhai Z, et al, . Meta-analysis of the association between nut consumption and the risks of cancer incidence and cancer-specific mortality. . 12:10772-10794. https://doi.org/10.18632/aging.103292

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                TY  - JOUR
                AU  - Zhang, Dai 
                AU  - Dai, Cong 
                AU  - Zhou, Linghui 
                AU  - Li, Yiche 
                AU  - Liu, Kang 
                AU  - Deng, Yu-Jiao 
                AU  - Li, Na 
                AU  - Zheng, Yi 
                AU  - Hao, Qian 
                AU  - Yang, Si 
                AU  - Song, Dingli 
                AU  - Wu, Ying 
                AU  - Zhai, Zhen 
                AU  - Cao, Shiyi 
                AU  - Dai, Zhijun 
                TI  - Meta-analysis of the association between nut consumption and the risks of cancer incidence and cancer-specific mortality
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103292
                DO  - 10.18632/aging.103292
                SP  - 10772
                EP  - 10794
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Zhang, Dai 
                AU  - Dai, Cong 
                AU  - Zhou, Linghui 
                AU  - Li, Yiche 
                AU  - Liu, Kang 
                AU  - Deng, Yu-Jiao 
                AU  - Li, Na 
                AU  - Zheng, Yi 
                AU  - Hao, Qian 
                AU  - Yang, Si 
                AU  - Song, Dingli 
                AU  - Wu, Ying 
                AU  - Zhai, Zhen 
                AU  - Cao, Shiyi 
                AU  - Dai, Zhijun 
                TI  - Meta-analysis of the association between nut consumption and the risks of cancer incidence and cancer-specific mortality
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103292
                DO  - 10.18632/aging.103292
                SP  - 10772
                EP  - 10794
                PY  - 
                AB  - Previous studies have indicated a correlation between nut intake and cancer risk in humans. This meta-analysis aimed to determine the relationship between nut consumption and the risks of cancer incidence and mortality. The PubMed, Embase, and Web of Science databases were searched up to August 2019. Relative risks and 95% confidence intervals were calculated using random-effects and fixed-effects models. We included 38 studies on nut consumption and cancer risk and 9 studies on cancer-specific mortality. Compared with no nut intake, nut intake was associated with a lower cancer risk (Relative Risk=0.90; 95% confidence interval, 0.86&#x2013;0.94). Inverse associations were observed with colorectal cancer, gastric cancer, pancreatic cancer, and lung cancer in subgroup analyses. Tree nut consumption was found to reduce cancer risk (Relative Risk=0.88; 95% confidence interval, 0.79&#x2013;0.99). Dose-response curves suggested that protective benefits against cancer increased with increased nut intake (P=0.005, P-nonlinearity=0.0414). An inverse correlation with cancer-specific mortality (Odd Ratio=0.90; 95% confidence interval, 0.88&#x2013;0.92) was observed. In conclusion, nut consumption is inversely associated with the risks of cancer incidence and mortality; a higher intake is significantly associated with a lower cancer risk.
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Association of gut microbiota composition and function with an aged rat model of senile osteoporosis using 16S rRNA and metagenomic sequencing analysis

Sicong Ma, Jinhong Qin, Yongqiang Hao, Lingjie Fu,

https://doi.org/10.18632/aging.103293 pp 10795—10808

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Ma S, Qin J, Hao Y, Fu L, . Association of gut microbiota composition and function with an aged rat model of senile osteoporosis using 16S rRNA and metagenomic sequencing analysis. . 12:10795-10808. https://doi.org/10.18632/aging.103293

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                TY  - JOUR
                AU  - Ma, Sicong 
                AU  - Qin, Jinhong 
                AU  - Hao, Yongqiang 
                AU  - Fu, Lingjie 
                TI  - Association of gut microbiota composition and function with an aged rat model of senile osteoporosis using 16S rRNA and metagenomic sequencing analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103293
                DO  - 10.18632/aging.103293
                SP  - 10795
                EP  - 10808
                PY  - 
                AB  - Recently, more interest has been paid to the association between bone mass and gut microecological dysbiosis. The results of clinical studies comparing gut microbiota (GM) in osteoporosis patients have been inconsistent due to different inclusion and exclusion criteria. To date, the association between the GM and senile osteoporosis remains poorly understood. Here, we utilized an aged rat model (22 months old) of senile osteoporosis to study the association of the composition and function of the GM with osteoporosis by 16S rRNA and metagenomic sequencing. The results showed that there was a significant reduction in alpha diversity and the F/B (Firmicutes/Bacteroidetes) ratio in aged rats. At the genus level, the enrichment of Helicobacter was potentially related to osteoporosis as a risk factor. Metagenomics results based on two databases indicated that shifts in the GM contribute to senile osteoporosis through metabolic pathways and subsequent immune disorders. In conclusion, our study reveals the association of gut microbiota composition and function with senile osteoporosis in an aged rat model in a brand new way, and variations in the GM might contribute to senile osteoporosis through metabolic pathways.
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LncRNA and mRNA expression profiles reveal the potential roles of lncRNA contributing to regulating dural penetration in clival chordoma

Jiwei Bai, Yixuan Zhai, Shuai Wang, Mingxuan Li, Shuheng Zhang, Chuzhong Li, Songbai Gui, Qi Li, Yazhuo Zhang,

https://doi.org/10.18632/aging.103294 pp 10809—10826

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Bai J, Zhai Y, Wang S, Li M, Zhang S, Li C, Gui S, Li Q, Zhang Y, . LncRNA and mRNA expression profiles reveal the potential roles of lncRNA contributing to regulating dural penetration in clival chordoma. . 12:10809-10826. https://doi.org/10.18632/aging.103294

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                TY  - JOUR
                AU  - Bai, Jiwei 
                AU  - Zhai, Yixuan 
                AU  - Wang, Shuai 
                AU  - Li, Mingxuan 
                AU  - Zhang, Shuheng 
                AU  - Li, Chuzhong 
                AU  - Gui, Songbai 
                AU  - Li, Qi 
                AU  - Zhang, Yazhuo 
                TI  - LncRNA and mRNA expression profiles reveal the potential roles of lncRNA contributing to regulating dural penetration in clival chordoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103294
                DO  - 10.18632/aging.103294
                SP  - 10809
                EP  - 10826
                PY  - 
                AB  - Chordoma is a rare bone cancer originating from embryologic notochordal remnants. Clival chordomas show different dural penetration ability, with serious dural penetration exhibiting poorer prognosis. The molecular mechanism of dural penetration is not clear. We analyzed lncRNA and mRNA profiles in 12 chordoma patients with different degrees of dural penetration using expression microarrays. The differentially expressed lncRNAs and mRNAs were used to construct a lncRNA-mRNA co-expression network. LncRNAs were classified into lincRNA, enhancer-like lncRNA, or antisense lncRNA. Biological functions for lncRNAs were predicted according to the lncRNA-mRNA network and adjacent coding genes by pathway analysis. The 2760 lncRNAs and 3988 mRNAs were differentially expressed in chordomas between two groups of patients with and without dural penetration. Possible pathway involvement of the significance among the 55 lncRNAs located in the lncRNA-mRNA network, 24 lincRNAs, 7 enhancer-like lncRNAs, and 14 antisense lncRNAs include cell adhesion, metastasis, invasion, proliferation, and apoptosis. Expression of 10 lncRNAs and mRNAs, and epidermal growth factor mRNA with two identified lncRNAs were subsequently verified by qRT-PCR in chordoma tissues. Our report predicts the biological functions of many lncRNAs which may be used as diagnostic and prognostic biomarkers as well as therapeutic targets during the process of dural penetration in chordoma.
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High mutation load, immune-activated microenvironment, favorable outcome, and better immunotherapeutic efficacy in melanoma patients harboring MUC16/CA125 mutations

Qinghua Wang, Yichen Yang, Meng Yang, Xiangchun Li, Kexin Chen,

https://doi.org/10.18632/aging.103296 pp 10827—10843

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Wang Q, Yang Y, Yang M, Li X, Chen K, . High mutation load, immune-activated microenvironment, favorable outcome, and better immunotherapeutic efficacy in melanoma patients harboring MUC16/CA125 mutations. . 12:10827-10843. https://doi.org/10.18632/aging.103296

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Provider: 
 TY - JOUR
 AU - Wang, Qinghua 
 AU - Yang, Yichen 
 AU - Yang, Meng 
 AU - Li, Xiangchun 
 AU - Chen, Kexin 
 TI - High mutation load, immune-activated microenvironment, favorable outcome, and better immunotherapeutic efficacy in melanoma patients harboring MUC16/CA125 mutations
 JO - 
 JA - 
 VL - 12
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103296
 DO - 10.18632/aging.103296
 SP - 10827
 EP - 10843
 PY - 
 AB - Immunotherapies have dramatically improved survival outcome for patients with melanoma. MUC16 encodes cancer antigen 125 (CA125), which is frequently mutated in melanoma. In this study, we correlated the MUC16 mutational status with the following: tumor mutation burden (TML), multiple immune-related signals in microenvironment, deregulated pathways, survival outcome, and immunotherapeutic efficacy. We found that patients with MUC16 mutations had significantly higher TML than those without it. Enriched pro-inflammatory CD8 T cells and M1 macrophages, enhanced interferon gamma (IFN&#x3B3;) and T cell-inflamed signatures, and increased cytolytic activity were associated with MUC16 mutations. Immune-suppressive M2 macrophages were enriched in patients with wild-type MUC16. Immune checkpoints expression (e.g., PD-L1, PD-1 and CTLA-4) was also elevated in patients with MUC16 mutations. Immune response relevant circuits were among the top enriched pathways in samples with MUC16 mutations. Patients with MUC16 mutations exhibited a significantly better prognosis. For patients who received immunotherapy, the presence of MUC16 mutations was associated with a better response rate and survival outcome in male patients but not in female or overall patients. These findings provide new implications for tailoring immunotherapeutic strategies for melanoma patients.
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Aberrantly glycosylated integrin α3β1 is a unique urinary biomarker for the diagnosis of bladder cancer

Di Jin, Ruiyun Zhang, Haige Chen, Chong Li,

https://doi.org/10.18632/aging.103297 pp 10844—10862

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Jin D, Zhang R, Chen H, Li C, . Aberrantly glycosylated integrin α3β1 is a unique urinary biomarker for the diagnosis of bladder cancer. . 12:10844-10862. https://doi.org/10.18632/aging.103297

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                TY  - JOUR
                AU  - Jin, Di 
                AU  - Zhang, Ruiyun 
                AU  - Chen, Haige 
                AU  - Li, Chong 
                TI  - Aberrantly glycosylated integrin α3β1 is a unique urinary biomarker for the diagnosis of bladder cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103297
                DO  - 10.18632/aging.103297
                SP  - 10844
                EP  - 10862
                PY  - 
                AB  - Bladder cancer (BC) is the most common malignancy of the urinary tract. We developed a new and ELISA kit for detecting aberrantly glycosylated integrin &#x3B1;3&#x3B2;1 (AG31) in human urine. We analysed urine samples (n=408) of patients with BC, renal cell carcinoma (RCC), prostate cancer (PC), cystitis, nephritis, and prostatitis from two centres in China. The subjects in the validation groups (n=2317) were recruited from other centres in China between July 2012 and September 2013. Receiver operating characteristic (ROC) curves were used to determine diagnostic accuracy. AG31 levels in urine samples were significantly higher in patients with BC than in any of the control subjects. Moreover, elevated levels of AG31 in urine could distinguish BC from benign inflammatory diseases. Finally, the urinary AG31 test was much more sensitive and specific than the NMP22 test. Therefore, the urinary AG31 test will provide an ideal and assay for the detection of BCs.
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Association between renal function impairment and multivessel involvement in patients with acute ST-elevation myocardial infarction

Rei-Yeuh Chang, Han-Lin Tsai, Malcolm Koo, How-Ran Guo,

https://doi.org/10.18632/aging.103299 pp 10863—10872

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Chang R, Tsai H, Koo M, Guo H, . Association between renal function impairment and multivessel involvement in patients with acute ST-elevation myocardial infarction. . 12:10863-10872. https://doi.org/10.18632/aging.103299

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                TY  - JOUR
                AU  - Chang, Rei-Yeuh 
                AU  - Tsai, Han-Lin 
                AU  - Koo, Malcolm 
                AU  - Guo, How-Ran 
                TI  - Association between renal function impairment and multivessel involvement in patients with acute ST-elevation myocardial infarction
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103299
                DO  - 10.18632/aging.103299
                SP  - 10863
                EP  - 10872
                PY  - 
                AB  - The aim of this study was to evaluate the association between acute ST-elevation myocardial infarction (STEMI) involving multivessel and the severity of renal function impairment. We reviewed medical records of patients with acute STEMI admitted to a regional teaching hospital in southern Taiwan between March 1999 and October 2013. A total of 1215 patients who underwent coronary angiography were included. Multiple logistic regression analysis showed that multivessel involvement (at least two) with significant stenosis was significantly associated with stage 4 chronic kidney disease (adjusted odds ratio [aOR]=2.14, 95% confidence interval [CI]=1.09&#x2013;4.20) and stage 5 chronic kidney disease (aOR=2.35, 95% CI=1.13&#x2013;4.89), adjusting for age, sex, type 2 diabetes mellitus, hyperlipidemia, and systolic blood pressure at admission in patients with acute STEMI. In addition, multivessel total occlusion was significantly associated with stage 4 chronic kidney disease (aOR=3.68, 95% CI=1.27&#x2013;10.70) and stage 5 chronic kidney disease (aOR=3.43, 95% CI=1.08&#x2013;10.82), adjusting for heart rate at admission and systolic blood pressure at admission in patients with acute STEMI. In conclusion, severe renal function impairment was significantly associated with multivessel significant stenosis and multivessel total occlusion in patients with acute STEMI.
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miR-137 prevents inflammatory response, oxidative stress, neuronal injury and cognitive impairment via blockade of Src-mediated MAPK signaling pathway in ischemic stroke

Runhui Tian, Bo Wu, Cong Fu, Kaimin Guo,

https://doi.org/10.18632/aging.103301 pp 10873—10895

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Tian R, Wu B, Fu C, Guo K, . miR-137 prevents inflammatory response, oxidative stress, neuronal injury and cognitive impairment via blockade of Src-mediated MAPK signaling pathway in ischemic stroke. . 12:10873-10895. https://doi.org/10.18632/aging.103301

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 TY - JOUR
 AU - Tian, Runhui 
 AU - Wu, Bo 
 AU - Fu, Cong 
 AU - Guo, Kaimin 
 TI - miR-137 prevents inflammatory response, oxidative stress, neuronal injury and cognitive impairment via blockade of Src-mediated MAPK signaling pathway in ischemic stroke
 JO - 
 JA - 
 VL - 12
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103301
 DO - 10.18632/aging.103301
 SP - 10873
 EP - 10895
 PY - 
 AB - Stroke is a leading cause of death and disability worldwide. The purpose of this study was to investigate the possible role of the microRNA (miRNA or miR) miR-137 in ischemic stroke. miRNAs are very stable in the blood and may serve as potential diagnostic and therapeutic markers. Wild-type, Src-/- and miR-137-/- mice were treated with p38 siRNA or Erk2 siRNA to identify their roles in the inflammatory response, oxidative stress, neuronal injury and cognitive impairment in brain tissues of mice following middle cerebral artery occlusion (MCAO) operation. We evaluated several factors including; inflammatory responses, oxidative stress, viability and apoptosis of astrocytes in order to identify the functions of miR-137 and Src in ischemic stroke. miR-137 alleviated the inflammatory response, oxidative stress, neuronal injury and cognitive impairment, and restricted apoptosis via targeting Src and inactivating the MAPK signaling pathway. Furthermore, up-regulation of miR-137 or inhibition of Src inhibited the secretion of inflammatory factors, suppressed oxidative stress, and reduced apoptosis of astrocytes. In conclusion, our work suggests that, in mice, miR-137 confers neuroprotective effects against ischemic stroke via attenuation of oxidative, apoptotic, and inflammatory pathways through inhibiting Src-dependent MAPK signaling pathway.
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SPTBN1 suppresses the progression of epithelial ovarian cancer via SOCS3-mediated blockade of the JAK/STAT3 signaling pathway

Mo Chen, Jia Zeng, Shuyi Chen, Jiajia Li, Huijie Wu, Xuhui Dong, Yuan Lei, Xiuling Zhi, Liangqing Yao,

https://doi.org/10.18632/aging.103303 pp 10896—10911

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Chen M, Zeng J, Chen S, Li J, Wu H, Dong X, Lei Y, Zhi X, Yao L, . SPTBN1 suppresses the progression of epithelial ovarian cancer via SOCS3-mediated blockade of the JAK/STAT3 signaling pathway. . 12:10896-10911. https://doi.org/10.18632/aging.103303

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                TY  - JOUR
                AU  - Chen, Mo 
                AU  - Zeng, Jia 
                AU  - Chen, Shuyi 
                AU  - Li, Jiajia 
                AU  - Wu, Huijie 
                AU  - Dong, Xuhui 
                AU  - Lei, Yuan 
                AU  - Zhi, Xiuling 
                AU  - Yao, Liangqing 
                TI  - SPTBN1 suppresses the progression of epithelial ovarian cancer via SOCS3-mediated blockade of the JAK/STAT3 signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103303
                DO  - 10.18632/aging.103303
                SP  - 10896
                EP  - 10911
                PY  - 
                AB  - SPTBN1 plays an anticancer role in many kinds of tumors and participates in the chemotherapeutic resistance of epithelial ovarian cancer (EOC). Here, we reported that lower SPTBN1 expression was significantly related to advanced EOC stage and shorter progression-free survival. SPTBN1 expression was also higher in less invasive EOC cell lines. Moreover, SPTBN1 decreased the migration ability of the EOC cells A2780 and HO8910 and inhibited the growth of EOC cells in vitro and tumor xenografts in vivo. SPTBN1 suppression increased the epithelial mesenchymal transformation marker Vimentin while decreasing E-cadherin expression. By analyzing TCGA data and immunohistochemistry staining of tumor tissue, we found that SPTBN1 and SOCS3 were positively coexpressed in EOC patients. SOCS3 overexpression or JAK2 inhibition decreased the proliferation and migration of EOC cells as well as the expression of p-JAK2, p-STAT3 and Vimentin, which were enhanced by the downregulation of SPTBN1, while E-cadherin expression was also reversed. It was also verified in mouse embryonic fibroblasts (MEFs) that loss of SPTBN1 activated the JAK/STAT3 signaling pathway with suppression of SOCS3. Our results suggest that SPTBN1 suppresses the progression of epithelial ovarian cancer via SOCS3-mediated blockade of the JAK/STAT3 signaling pathway.
                ER  -

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Dynamic changes of autophagic flux induced by Abeta in the brain of postmortem Alzheimer’s disease patients, animal models and cell models

Zhimin Long, Jingfei Chen, Yueyang Zhao, Wen Zhou, Qiuhui Yao, Yingxiong Wang, Guiqiong He,

https://doi.org/10.18632/aging.103305 pp 10912—10930

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Long Z, Chen J, Zhao Y, Zhou W, Yao Q, Wang Y, He G, . Dynamic changes of autophagic flux induced by Abeta in the brain of postmortem Alzheimer’s disease patients, animal models and cell models. . 12:10912-10930. https://doi.org/10.18632/aging.103305

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                TY  - JOUR
                AU  - Long, Zhimin 
                AU  - Chen, Jingfei 
                AU  - Zhao, Yueyang 
                AU  - Zhou, Wen 
                AU  - Yao, Qiuhui 
                AU  - Wang, Yingxiong 
                AU  - He, Guiqiong 
                TI  - Dynamic changes of autophagic flux induced by Abeta in the brain of postmortem Alzheimer’s disease patients, animal models and cell models
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103305
                DO  - 10.18632/aging.103305
                SP  - 10912
                EP  - 10930
                PY  - 
                AB  - Autophagy has been reported to play a dual &quot;double-edged sword&quot; role in the occurrence and development of Alzheimer&#x2019;s disease (AD). To assess the relationship between AD and autophagy, the dynamic changes of autophagic flux in the brain of postmortem AD patients, animal models and cell models were studied. The results showed that autophagosomes (APs) accumulation and expression of lysosomal markers were decreased in the brains of AD patients. In the brain of APP/PS1 double transgenic mice, APs did not accumulate before the formation of SPs but accumulated along with the deposition of SPs, as well as the level of lysosomal markers cathepsin B and Lamp1 protein decreased significantly. In the brains of APP/PS1/LC3 triple - transgenic mice, the number of APs increased with age, but the number of ALs did not increase accordingly. The activation of autophagy is mainly due to the increase in A&#x3B2; rather than the overexpression of mutated APP gene. However, both the treatment with exogenous A&#x3B2;25-35 and the mutation of the endogenous APP gene blocked the fusion of APs with lysosomes and decreased lysosomal functioning in AD model cells, which may be the main mechanism of autophagy dysregulation in AD.
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Hypoxia-preconditioned olfactory mucosa mesenchymal stem cells abolish cerebral ischemia/reperfusion-induced pyroptosis and apoptotic death of microglial cells by activating HIF-1α

Yan Huang, Fengbo Tan, Yi Zhuo, Jianyang Liu, Jialin He, Da Duan, Ming Lu, Zhiping Hu,

https://doi.org/10.18632/aging.103307 pp 10931—10950

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Huang Y, Tan F, Zhuo Y, Liu J, He J, Duan D, Lu M, Hu Z, . Hypoxia-preconditioned olfactory mucosa mesenchymal stem cells abolish cerebral ischemia/reperfusion-induced pyroptosis and apoptotic death of microglial cells by activating HIF-1α. . 12:10931-10950. https://doi.org/10.18632/aging.103307

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                TY  - JOUR
                AU  - Huang, Yan 
                AU  - Tan, Fengbo 
                AU  - Zhuo, Yi 
                AU  - Liu, Jianyang 
                AU  - He, Jialin 
                AU  - Duan, Da 
                AU  - Lu, Ming 
                AU  - Hu, Zhiping 
                TI  - Hypoxia-preconditioned olfactory mucosa mesenchymal stem cells abolish cerebral ischemia/reperfusion-induced pyroptosis and apoptotic death of microglial cells by activating HIF-1α
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103307
                DO  - 10.18632/aging.103307
                SP  - 10931
                EP  - 10950
                PY  - 
                AB  - Microglial cells are the first line immune cells that initiate inflammatory responses following cerebral ischemia/reperfusion(I/R) injury. Microglial cells are also associated with a novel subtype of pro-inflammatory programmed cell death known as pyroptosis. Research has been directed at developing treatments that modulate inflammatory responses and protect against cell death caused by cerebral I/R. Key among such treatments include mesenchymal stem cell (MSC) therapy. A unique type of MSC termed olfactory mucosa mesenchymal stem cell (OM-MSC) confers neuroprotection by promoting the secretion of paracrine factors, and neuroprotection. This study investigated whether hypoxic OM-MSCs could inhibit microglial cell death upon I/R insult in vitro. A traditional oxygen-glucose deprivation/reperfusion (OGD/R) model, analogous to I/R, was established. Results showed that OGD/R induced apoptosis and pyroptosis in microglial cells while hypoxia in OM-MSCs significantly attenuated these effects. Moreover, the effects of OM-MSCs were mediated by Hypoxia-inducible factor 1-alpha (HIF-1&#x3B1;). Taken together, these findings reveal that hypoxia-preconditioned OM-MSC inhibits pyroptotic and apoptotic death of microglial cell in response to cerebral ischemia/reperfusion insult by activating HIF-1&#x3B1; in vitro.
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Fibroblast growth factor 2 contributes to the effect of salidroside on dendritic and synaptic plasticity after cerebral ischemia/reperfusion injury

Sisi Li, Yechen Lu, Daofang Ding, Zhenzhen Ma, Xiangxin Xing, Xuyun Hua, Jianguang Xu,

https://doi.org/10.18632/aging.103308 pp 10951—10968

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Li S, Lu Y, Ding D, Ma Z, Xing X, Hua X, Xu J, . Fibroblast growth factor 2 contributes to the effect of salidroside on dendritic and synaptic plasticity after cerebral ischemia/reperfusion injury. . 12:10951-10968. https://doi.org/10.18632/aging.103308

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                TY  - JOUR
                AU  - Li, Sisi 
                AU  - Lu, Yechen 
                AU  - Ding, Daofang 
                AU  - Ma, Zhenzhen 
                AU  - Xing, Xiangxin 
                AU  - Hua, Xuyun 
                AU  - Xu, Jianguang 
                TI  - Fibroblast growth factor 2 contributes to the effect of salidroside on dendritic and synaptic plasticity after cerebral ischemia/reperfusion injury
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103308
                DO  - 10.18632/aging.103308
                SP  - 10951
                EP  - 10968
                PY  - 
                AB  - Ischemic stroke, a serious neurological disease, is associated with cell death, axonal and dendritic plasticity, and other activities. Anti-inflammatory, anti-apoptotic, promote dendritic and synaptic plasticity are critical therapeutic targets after ischemic stroke. Fibroblast growth factor-2 (FGF2), which is involved in the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/CAMP response element (CRE)-binding protein (CREB) pathway, has been shown to facilitate dendritic and synaptic plasticity. Salidroside (Sal) has been reported to have anti-inflammatory, anti-oxidative, and anti-apoptotic effects; however, the underlying mechanisms of Sal in promoting dendritic and synaptic plasticity remain unclear. Here, the anti-inflammatory, anti-apoptotic, dendritic and synaptic plasticity effects of Sal were investigated in vitro in PC12 cells under oxygen-glucose deprivation/reoxygenation (OGD/R) conditions and in vivo in rats with middle cerebral artery occlusion/reperfusion (MCAO/R). We investigated the role of Sal in promoting dendritic and synaptic plasticity in the ischemic penumbra and whether the FGF2-mediated cAMP/PKA/CREB pathway was involved in this process. The present study demonstrated that Sal could significantly inhibit inflammation and apoptosis, and promote dendritic and synaptic plasticity. Overall, our study suggests that Sal is an effective treatment for ischemic stroke that functions via the FGF2-mediated cAMP/PKA/CREB pathway to promote dendritic and synaptic plasticity.
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P22077 inhibits LPS-induced inflammatory response by promoting K48-linked ubiquitination and degradation of TRAF6

Xi-Bao Zhao, Fei-Yang Ji, Hong-Rui Li, Hui-Hui Zhu, Zi-Zhao Zhao, Jing Ling, Qian-Qian Di, Xing-Yu Ma, Wei-Lin Chen,

https://doi.org/10.18632/aging.103309 pp 10969—10982

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Zhao X, Ji F, Li H, Zhu H, Zhao Z, Ling J, Di Q, Ma X, Chen W, . P22077 inhibits LPS-induced inflammatory response by promoting K48-linked ubiquitination and degradation of TRAF6. . 12:10969-10982. https://doi.org/10.18632/aging.103309

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                TY  - JOUR
                AU  - Zhao, Xi-Bao 
                AU  - Ji, Fei-Yang 
                AU  - Li, Hong-Rui 
                AU  - Zhu, Hui-Hui 
                AU  - Zhao, Zi-Zhao 
                AU  - Ling, Jing 
                AU  - Di, Qian-Qian 
                AU  - Ma, Xing-Yu 
                AU  - Chen, Wei-Lin 
                TI  - P22077 inhibits LPS-induced inflammatory response by promoting K48-linked ubiquitination and degradation of TRAF6
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103309
                DO  - 10.18632/aging.103309
                SP  - 10969
                EP  - 10982
                PY  - 
                AB  - Inflammation is a biological process associated with multiple human disorders such as autoimmune diseases and metabolic diseases. Therefore, alleviation of inflammation is important for disease prevention or treatment. Recently, deubiquitinating enzymes (DUBs), especially ubiquitin specific protease-7 (USP7) attracts increasing attention as a potential drug target for inflammation. As an inhibitor of USP7, P22077 has been used to study the roles of USP7 in inflammatory response and neuroblastoma growth. However, the role and precise mechanism of P22077 in anti-inflammatory is still indistinct. In this study, we demonstrated that P22077 could attenuate the release of pro-inflammatory factors including TNF-&#x3B1;, IL-1&#x3B2;, IL-6 and NO, suppress mRNA expression of COX-2 and iNOS, and inhibit activation of NF-&#x3BA;B and MAPKs signaling pathways in Raw264.7 cells and mouse peritoneal macrophages after LPS stimulation. In vivo study showed that P22077 could relieve inflammatory response and reduce the lung injury in C57BL/6 mice with LPS-induced endotoxemia. Mechanically, P22077 might play an anti-inflammatory role by promoting tumor necrosis factor receptor-associated factor 6 (TRAF6) degradation via K48-linked polyubiquitination. These findings provide a rationale for the role of the P22077 in anti-inflammatory pathway and the promising clinical application of P22077 to treat inflammatory diseases.
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The circRNA circIFI30 promotes progression of triple-negative breast cancer and correlates with prognosis

Lei Xing, Rui Yang, Xiaosong Wang, Xiaying Zheng, Xin Yang, Luyu Zhang, Rong Jiang, Guosheng Ren, Junxia Chen,

https://doi.org/10.18632/aging.103311 pp 10983—11003

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Xing L, Yang R, Wang X, Zheng X, Yang X, Zhang L, Jiang R, Ren G, Chen J, . The circRNA circIFI30 promotes progression of triple-negative breast cancer and correlates with prognosis. . 12:10983-11003. https://doi.org/10.18632/aging.103311

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                TY  - JOUR
                AU  - Xing, Lei 
                AU  - Yang, Rui 
                AU  - Wang, Xiaosong 
                AU  - Zheng, Xiaying 
                AU  - Yang, Xin 
                AU  - Zhang, Luyu 
                AU  - Jiang, Rong 
                AU  - Ren, Guosheng 
                AU  - Chen, Junxia 
                TI  - The circRNA circIFI30 promotes progression of triple-negative breast cancer and correlates with prognosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103311
                DO  - 10.18632/aging.103311
                SP  - 10983
                EP  - 11003
                PY  - 
                AB  - Growing evidence suggests that circRNAs exert a critical role in tumorigenesis and cancer progression. To date, the molecular mechanisms underlying circRNAs in triple-negative breast cancer (TNBC) are still poorly known. Here, circRNA expression profile was investigated by RNA sequencing in TNBC tissues and matched para-carcinoma tissues. We found that circIFI30 was significantly up-regulated in TNBC tissues and cells using quantitative real-time PCR and in situ hybridization. High circIFI30 expression was positively correlated with clinical TNM stage, pathological grade and poor prognosis of TNBC patients. Functionally, a series of in vivo and in vitro experiments showed that knockdown of circIFI30 could markedly inhibit TNBC cell proliferation, migration, invasion and cell cycle progression, induce apoptosis as well as suppress tumorigenesis and metastasis. Up-regulation of circIFI30 exerted an opposite effect. Mechanistically, we demonstrated that circIFI30 might act as a competing endogenous RNA (ceRNA) of miR-520b-3p to abolish the suppressive effect on target gene CD44 by fluorescent in situ hybridization (FISH), dual luciferase reporter assay, RNA immunoprecipitation and RNA pull-down assays. Therefore, our work uncovers the mechanism by which circIFI30 could promote TNBC progression through circIFI30/miR-520b-3p/CD44 axis and circIFI30 could be a novel diagnostic/prognostic marker and therapeutic target for TNBC patients.
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Upregulation of Mlxipl induced by cJun in the spinal dorsal horn after peripheral nerve injury counteracts mechanical allodynia by inhibiting neuroinflammation

Hongrui Zhan, Yaping Wang, Shi Yu, Guiyuan Cai, Yanyan Zeng, Junqin Ma, Wei Liu, Wen Wu,

https://doi.org/10.18632/aging.103313 pp 11004—11024

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Zhan H, Wang Y, Yu S, Cai G, Zeng Y, Ma J, Liu W, Wu W, . Upregulation of Mlxipl induced by cJun in the spinal dorsal horn after peripheral nerve injury counteracts mechanical allodynia by inhibiting neuroinflammation. . 12:11004-11024. https://doi.org/10.18632/aging.103313

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                TY  - JOUR
                AU  - Zhan, Hongrui 
                AU  - Wang, Yaping 
                AU  - Yu, Shi 
                AU  - Cai, Guiyuan 
                AU  - Zeng, Yanyan 
                AU  - Ma, Junqin 
                AU  - Liu, Wei 
                AU  - Wu, Wen 
                TI  - Upregulation of Mlxipl induced by cJun in the spinal dorsal horn after peripheral nerve injury counteracts mechanical allodynia by inhibiting neuroinflammation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103313
                DO  - 10.18632/aging.103313
                SP  - 11004
                EP  - 11024
                PY  - 
                AB  - Mlxipl regulates glucose metabolism, lipogenesis and tumorigenesis and has a wide-ranging impact on human health and disease. However, the role of Mlxipl in neuropathic pain remains unknown. In this study, we found that Mlxipl was increased in the ipsilateral L4&#x2013;L6 spinal dorsal horn after Spared Nerve Injury surgery. Knockdown of Mlxipl in the ipsilateral L4&#x2013;L6 spinal dorsal horn by intraspinal microinjection aggravated Spared Nerve Injury-induced mechanical allodynia and inflammation in the spinal dorsal horn, on the contrary, overexpression of Mlxipl inhibited mechanical allodynia and inflammation. Subsequently, the rat Mlxipl promoter was analyzed using bioinformatics methods to predict the upstream transcription factor cJun. Luciferase assays and ChIP-qPCR confirmed that cJun bound to the promoter of Mlxipl and enhanced its expression. Finally, we demonstrated that Mlxipl inhibited the inflammatory responses of lipopolysaccharide-induced microglia and that Mlxipl was regulated by the transcription factor cJun. These findings suggested that cJun-induced Mlxipl upregulation in the spinal dorsal horn after peripheral nerve injury provided a protective mechanism for the development and progression of neuropathic pain by inhibiting microglial-derived neuroinflammation. Targeting Mlxipl in the spinal dorsal horn might represent an effective strategy for the treatment of neuropathic pain.
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LncRNA ADAMTS9-AS2 inhibits gastric cancer (GC) development and sensitizes chemoresistant GC cells to cisplatin by regulating miR-223-3p/NLRP3 axis

Niansheng Ren, Tao Jiang, Chengbo Wang, Shilin Xie, Yanwei Xing, Daxun Piao, Tiemin Zhang, Yuekun Zhu,

https://doi.org/10.18632/aging.103314 pp 11025—11041

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Ren N, Jiang T, Wang C, Xie S, Xing Y, Piao D, Zhang T, Zhu Y, . LncRNA ADAMTS9-AS2 inhibits gastric cancer (GC) development and sensitizes chemoresistant GC cells to cisplatin by regulating miR-223-3p/NLRP3 axis. . 12:11025-11041. https://doi.org/10.18632/aging.103314

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                TY  - JOUR
                AU  - Ren, Niansheng 
                AU  - Jiang, Tao 
                AU  - Wang, Chengbo 
                AU  - Xie, Shilin 
                AU  - Xing, Yanwei 
                AU  - Piao, Daxun 
                AU  - Zhang, Tiemin 
                AU  - Zhu, Yuekun 
                TI  - LncRNA ADAMTS9-AS2 inhibits gastric cancer (GC) development and sensitizes chemoresistant GC cells to cisplatin by regulating miR-223-3p/NLRP3 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103314
                DO  - 10.18632/aging.103314
                SP  - 11025
                EP  - 11041
                PY  - 
                AB  - The role of LncRNA ADAMTS9-AS2 in the regulation of chemoresistance of gastric cancer (GC) is largely unknown. Here we found that LncRNA ADAMTS9-AS2 was low-expressed in GC tissues and cells compared to their normal counterparts. In addition, LncRNA ADAMTS9-AS2 inhibited miR-223-3p expressions in GC cells by acting as competing endogenous RNA, and the levels of LncRNA ADAMTS9-AS2 and miR-223-3p showed negative correlations in GC tissues. Of note, overexpression of LncRNA ADAMTS9-AS2 inhibited GC cell viability and motility by sponging miR-223-3p. In addition, the levels of LncRNA ADAMTS9-AS2 were lower, and miR-223-3p was higher in cisplatin-resistant GC (CR-GC) cells than their parental cisplatin-sensitive GC (CS-GC) cells. LncRNA ADAMTS9-AS2 overexpression enhanced the cytotoxic effects of cisplatin on CR-GC cells, which were reversed by overexpressing miR-223-3p. Furthermore, LncRNA ADAMTS9-AS2 increased NLRP3 expressions by targeting miR-223-3p, and upregulation of LncRNA ADAMTS9-AS2 triggered pyroptotic cell death in cisplatin treated CR-GC cells by activating NLRP3 inflammasome through downregulating miR-223-3p. Finally, the promoting effects of LncRNA ADAMTS9-AS2 overexpression on CR-GC cell death were abrogated by pyroptosis inhibitor Necrosulfonamide (NSA). Collectively, LncRNA ADAMTS9-AS2 acted as a tumor suppressor and enhanced cisplatin sensitivity in GC cells by activating NLRP3 mediated pyroptotic cell death through sponging miR-223-3p.
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Highly expressed STAT1 contributes to the suppression of stemness properties in human paclitaxel-resistant ovarian cancer cells

Fanchen Wang, Lingyun Zhang, Jiao Liu, Jinguo Zhang, Guoxiong Xu,

https://doi.org/10.18632/aging.103317 pp 11042—11060

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Wang F, Zhang L, Liu J, Zhang J, Xu G, . Highly expressed STAT1 contributes to the suppression of stemness properties in human paclitaxel-resistant ovarian cancer cells. . 12:11042-11060. https://doi.org/10.18632/aging.103317

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                TY  - JOUR
                AU  - Wang, Fanchen 
                AU  - Zhang, Lingyun 
                AU  - Liu, Jiao 
                AU  - Zhang, Jinguo 
                AU  - Xu, Guoxiong 
                TI  - Highly expressed STAT1 contributes to the suppression of stemness properties in human paclitaxel-resistant ovarian cancer cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103317
                DO  - 10.18632/aging.103317
                SP  - 11042
                EP  - 11060
                PY  - 
                AB  - Signal transducer and activator of transcription-1 (STAT1) is an important factor in various cellular processes. The cancer stem cell (CSC) is considered as a tumor-initiating cell that drives the inner hierarchy in many cancers including epithelial ovarian cancer (EOC). Here, we explored for the first time the regulation of STAT1 on stemness properties in chemoresistant EOC cells. The paclitaxel (PTX)-resistant EOC cell line (OV3R-PTX) was derived from PTX-sensitive OVCAR-3 cells treated by the PTX regimen. A single cell clone OV3R-PTX-B4 was selected by fluorescence-activated cell sorting. PTX-resistant cells grew slowly in conventional 2D and 3D cultures, but tumor xenograft with PTX-resistant cells grew fast in nude mice. Interestingly, OV3R-PTX-B4 cells shared the characteristics of CSCs and stemness properties were found to be increased in the non-adherent spheroid culture system. The PTX-resistant cells had a high expression of CSC-related markers and low expression of STAT1 that had a high methylation level of CpG in its promoter region. Overexpressed STAT1 suppressed stemness properties, cell proliferation, and colony formation and favored the overall survival of patients with EOC. In summary, these data indicate a regulatory mechanism of STAT1 underlying drug resistance and provide a potential therapeutic application for EOC patients with PTX resistance.
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T cell stimulation and expansion by SunTag-based clustering of anti-CD3/CD28 scFv

Kunhong Zhong, Zhiyong Liu, Hongjian Li, Shasha Zhao, Yuelong Wang, Wenhao Guo, Xi Zheng, Hui Yang, Gang Guo, Liangxue Zhou, Jianguo Xu, Aiping Tong,

https://doi.org/10.18632/aging.103318 pp 11061—11070

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Zhong K, Liu Z, Li H, Zhao S, Wang Y, Guo W, Zheng X, Yang H, Guo G, Zhou L, Xu J, Tong A, . T cell stimulation and expansion by SunTag-based clustering of anti-CD3/CD28 scFv. . 12:11061-11070. https://doi.org/10.18632/aging.103318

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                TY  - JOUR
                AU  - Zhong, Kunhong 
                AU  - Liu, Zhiyong 
                AU  - Li, Hongjian 
                AU  - Zhao, Shasha 
                AU  - Wang, Yuelong 
                AU  - Guo, Wenhao 
                AU  - Zheng, Xi 
                AU  - Yang, Hui 
                AU  - Guo, Gang 
                AU  - Zhou, Liangxue 
                AU  - Xu, Jianguo 
                AU  - Tong, Aiping 
                TI  - T cell stimulation and expansion by SunTag-based clustering of anti-CD3/CD28 scFv
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103318
                DO  - 10.18632/aging.103318
                SP  - 11061
                EP  - 11070
                PY  - 
                AB  - Therapeutic ex vivo T cell expansion is limited by low rates and poor functionality, especially for T cells from aged cancer patients. Here, we describe a novel method for T cell stimulation and expansion using a system named SunTag-based clustering of anti-CD3/CD28 scFv (SBCS). In this method, SunTag was used to recruit up to 13 copies of anti-CD3/CD28 scFv for T cell activation. Compared with the traditional method using immobilized CD3/CD28 antibodies, the SBCS system produced approximately 1.5-fold greater expansion of T cells from healthy donors, and more than 2-fold greater expansion of T cells from aged cancer patients after stimulation. The efficiency of expansion depended mainly on the concentration of the clustered polymers of anti-CD3 scFv rather than anti-CD28 scFv. We also demonstrated that the SBCS-expanded T cells could be used to prepare functional chimeric antigen receptor modified T cells for antitumor therapy.
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LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK

Gong Zhang, Ximin Chen, Lei Ma, Rui Ding, Lihong Zhao, Feng Ma, Xubin Deng,

https://doi.org/10.18632/aging.103321 pp 11071—11084

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Zhang G, Chen X, Ma L, Ding R, Zhao L, Ma F, Deng X, . LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK. . 12:11071-11084. https://doi.org/10.18632/aging.103321

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                TY  - JOUR
                AU  - Zhang, Gong 
                AU  - Chen, Ximin 
                AU  - Ma, Lei 
                AU  - Ding, Rui 
                AU  - Zhao, Lihong 
                AU  - Ma, Feng 
                AU  - Deng, Xubin 
                TI  - LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103321
                DO  - 10.18632/aging.103321
                SP  - 11071
                EP  - 11084
                PY  - 
                AB  - Long non-coding RNAs (lncRNAs) have been reported to play significant roles in human tumorigenesis, for example, in hepatocellular carcinoma (HCC). This study explored the role of LINC01419, a new lncRNA, in HCC. In vitro study revealed that LINC01419 promotes growth and migration of HCC cells. Genes that affected cell proliferation and cell migration were identified using RNA-sequence. Subsequently, it was confirmed that LINC01419 binds to EZH2, leading to histone methylation of the RECK promoter. Interaction between LINC01419 and FUS stabilized EZH2 mRNA thereby enhancing EZH2 expression. Conclusively, the results of this study confirm that LINC01419 may serve as a potential target for HCC diagnosis and treatment.
                ER  -

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The effect of swimming exercise and diet on the hypothalamic inflammation of ApoE-/- mice based on SIRT1-NF-κB-GnRH expression

Xialei Wang, Jingda Yang, Taotao Lu, Zengtu Zhan, Wei Wei, Xinru Lyu, Yijing Jiang, Xiehua Xue,

https://doi.org/10.18632/aging.103323 pp 11085—11099

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Wang X, Yang J, Lu T, Zhan Z, Wei W, Lyu X, Jiang Y, Xue X, . The effect of swimming exercise and diet on the hypothalamic inflammation of ApoE-/- mice based on SIRT1-NF-κB-GnRH expression. . 12:11085-11099. https://doi.org/10.18632/aging.103323

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                TY  - JOUR
                AU  - Wang, Xialei 
                AU  - Yang, Jingda 
                AU  - Lu, Taotao 
                AU  - Zhan, Zengtu 
                AU  - Wei, Wei 
                AU  - Lyu, Xinru 
                AU  - Jiang, Yijing 
                AU  - Xue, Xiehua 
                TI  - The effect of swimming exercise and diet on the hypothalamic inflammation of ApoE-/- mice based on SIRT1-NF-κB-GnRH expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103323
                DO  - 10.18632/aging.103323
                SP  - 11085
                EP  - 11099
                PY  - 
                AB  - A high-fat diet and sedentary lifestyle could accelerate aging and hypothalamic inflammation. In order to explore the regulatory mechanisms of lifestyle in the hypothalamus, swimming exercise and diet control were applied in the high-fat diet ApoE-/- mice in our study. 20-week-old ApoE-/- mice fed with 12-week high-fat diet were treated by high-fat diet, diet control and swimming exercise. The results showed that hypothalamic inflammation, glial cells activation and cognition decline were induced by high-fat diet. Compared with the diet control, hypothalamic inflammation, glial cells activation and learning and memory impairment were effectively alleviated by swimming exercise plus diet control, which was related to the increasing expression of SIRT1, inhibiting the expression of NF-&#x3BA;B and raising secretion of GnRH in the hypothalamus. These findings supported the hypothesis that hypothalamic inflammation was susceptible to exercise and diet, which was strongly associated with SIRT1-NF-&#x3BA;B-GnRH expression in the hypothalamus.
                ER  -

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ANXA7 promotes the cell cycle, proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells by up-regulating CDC5L

Haiyan Liu, Dan Guo, Yuou Sha, Chenlu Zhang, Yijing Jiang, Lemin Hong, Jie Zhang, Yuwen Jiang, Ling Lu, Hongming Huang,

https://doi.org/10.18632/aging.103326 pp 11100—11115

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Liu H, Guo D, Sha Y, Zhang C, Jiang Y, Hong L, Zhang J, Jiang Y, Lu L, Huang H, . ANXA7 promotes the cell cycle, proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells by up-regulating CDC5L. . 12:11100-11115. https://doi.org/10.18632/aging.103326

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                TY  - JOUR
                AU  - Liu, Haiyan 
                AU  - Guo, Dan 
                AU  - Sha, Yuou 
                AU  - Zhang, Chenlu 
                AU  - Jiang, Yijing 
                AU  - Hong, Lemin 
                AU  - Zhang, Jie 
                AU  - Jiang, Yuwen 
                AU  - Lu, Ling 
                AU  - Huang, Hongming 
                TI  - ANXA7 promotes the cell cycle, proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells by up-regulating CDC5L
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103326
                DO  - 10.18632/aging.103326
                SP  - 11100
                EP  - 11115
                PY  - 
                AB  - This study aimed to investigate whether annexin A7 (ANXA7) could promote the cell cycle, proliferation and cell adhesion-mediated drug resistance (CAM-DR) of multiple myeloma (MM) cells by up-regulating cell division cycle 5-like (CDC5L). As a result, ANXA7 expression was increased in the serum of MM patients and the expression of ANXA7 and CDC5L was also increased in MM cell lines. ANXA7 overexpression promoted the proliferation and cycle of U266 and RPMI8226 cells. The expression of proliferation cell nuclear antigen (PCNA), KI67, cyclin dependent kinase 1 (CDK1) and cyclinB1 in transfected cells was consistent with the changes of proliferation and cell cycle. In co-culture system of BMSC cells and MM cells, expression of CD44, ICAM1 and VCAM1 in MM cells was increased, which was further increased by ANXA7 overexpression. Bortezomib could increase the apoptosis of U266 and RPMI8226 cells. In co-culture system of BMSC cells and MM cells, the promotion effects of bortezomib on apoptosis of MM cells was decreased, which was further suppressed by ANXA7 overexpression. The above effects exerted by ANXA7 overexpression could be reversed by ANXA7 interference. Moreover, ANXA7 was proved to be combined with CDC5L. CDC5L interference could inhibit the promotion effects of ANXA7 overexpression on proliferation and cell cycle and inhibition effects of ANXA7 overexpression on apoptosis of MM cells treated with bortezomib in co-culture system. In conclusion, ANXA7 could promote the cell cycle, proliferation and CAM-DR of MM cells by up-regulating CDC5L.
                ER  -

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Deoxyelephantopin induces apoptosis via oxidative stress and enhances gemcitabine sensitivity in vitro and in vivo through targeting the NF-κB signaling pathway in pancreatic cancer

Daolin Ji, Xiangyu Zhong, Peng Huang, Pengcheng Kang, Kaiming Leng, Wangyang Zheng, Zhidong Wang, Yi Xu, Yunfu Cui,

https://doi.org/10.18632/aging.103327 pp 11116—11138

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Ji D, Zhong X, Huang P, Kang P, Leng K, Zheng W, Wang Z, Xu Y, Cui Y, . Deoxyelephantopin induces apoptosis via oxidative stress and enhances gemcitabine sensitivity in vitro and in vivo through targeting the NF-κB signaling pathway in pancreatic cancer. . 12:11116-11138. https://doi.org/10.18632/aging.103327

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Provider: 
 TY - JOUR
 AU - Ji, Daolin 
 AU - Zhong, Xiangyu 
 AU - Huang, Peng 
 AU - Kang, Pengcheng 
 AU - Leng, Kaiming 
 AU - Zheng, Wangyang 
 AU - Wang, Zhidong 
 AU - Xu, Yi 
 AU - Cui, Yunfu 
 TI - Deoxyelephantopin induces apoptosis via oxidative stress and enhances gemcitabine sensitivity in vitro and in vivo through targeting the NF-κB signaling pathway in pancreatic cancer
 JO - 
 JA - 
 VL - 12
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103327
 DO - 10.18632/aging.103327
 SP - 11116
 EP - 11138
 PY - 
 AB - Pancreatic cancer is a highly invasive malignant tumor of the digestive system with an unfavorable prognosis worldwide. This trait is thought to be largely attributed to chemoresistance. Chemotherapy is the only hope for patients with advanced pancreatic cancer. Therefore, seeking new effective chemotherapy drugs has become an urgent need. The purpose of our study was to explore whether deoxyelephantopin (DET), a sesquiterpene lactone, has a potential antitumor effect in pancreatic cancer. Additionally, the antitumor effects of DET alone or in combination with gemcitabine (GEM) and the potential mechanism of this combination were revealed. In vitro experiments showed that DET suppressed the proliferation, invasion and metastasis of pancreatic cancer cells, induced cell apoptosis via oxidative stress, and enhanced GEM sensitivity by inhibiting the NF-&#x3BA;B signaling pathway. Beyond that, in vivo experiments showed that DET not only inhibited pancreatic tumor growth and metastasis but also amplified the antitumor capacity of GEM, which was related to the downregulation of NF-&#x3BA;B and its downstream gene products. In summary, it is possible that DET could be developed as a single agent or combined with conventional chemotherapy drugs to improve the treatment of pancreatic cancer.
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Melatonin regulates mitochondrial dynamics and alleviates neuron damage in prion diseases

Xixi Zhang, Deming Zhao, Wei Wu, Syed Zahid Ali Shah, Mengyu Lai, Dongming Yang, Jie Li, Zhiling Guan, Wen Li, Hongli Gao, Huafen Zhao, Xiangmei Zhou, Lifeng Yang,

https://doi.org/10.18632/aging.103328 pp 11139—11151

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Zhang X, Zhao D, Wu W, Ali Shah SZ, Lai M, Yang D, Li J, Guan Z, Li W, Gao H, Zhao H, Zhou X, Yang L, . Melatonin regulates mitochondrial dynamics and alleviates neuron damage in prion diseases. . 12:11139-11151. https://doi.org/10.18632/aging.103328

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                TY  - JOUR
                AU  - Zhang, Xixi 
                AU  - Zhao, Deming 
                AU  - Wu, Wei 
                AU  - Ali Shah, Syed Zahid 
                AU  - Lai, Mengyu 
                AU  - Yang, Dongming 
                AU  - Li, Jie 
                AU  - Guan, Zhiling 
                AU  - Li, Wen 
                AU  - Gao, Hongli 
                AU  - Zhao, Huafen 
                AU  - Zhou, Xiangmei 
                AU  - Yang, Lifeng 
                TI  - Melatonin regulates mitochondrial dynamics and alleviates neuron damage in prion diseases
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103328
                DO  - 10.18632/aging.103328
                SP  - 11139
                EP  - 11151
                PY  - 
                AB  - Prion diseases are neurodegenerative diseases associated with neuron damage and behavioral disorders in animals and humans. Melatonin is a potent antioxidant and is used to treat a variety of diseases. We investigated the neuroprotective effect of melatonin on prion-induced damage in N2a cells. N2a cells were pretreated with 10 &#x3BC;M melatonin for 1 hour followed by incubation with 100 &#x3BC;M PrP106-126 for 24 hours. Melatonin markedly alleviated PrP106-126-induced apoptosis of N2a cells, and inhibited PrP106-126-induced mitochondrial abnormality and dysfunction, including mitochondrial fragmentation and overproduction of reactive oxygen species (ROS), suppression of ATP, reduced mitochondrial membrane potential (MMP), and altered mitochondrial dynamic proteins dynamin-related protein 1 (DRP1) and optic atrophy protein 1 (OPA1). Our findings identify that pretreatment with melatonin prevents the deleterious effects of PrPSc on mitochondrial function and dynamics, protects synapses and alleviates neuron damage. Melatonin could be a novel and effective medication in the therapy of prion diseases.
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LSEC model of aging

Laurent Grosse, Dmitry V. Bulavin,

https://doi.org/10.18632/aging.103492 pp 11152—11160

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Grosse L, Bulavin DV, . LSEC model of aging. . 12:11152-11160. https://doi.org/10.18632/aging.103492

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                TY  - JOUR
                AU  - Grosse, Laurent 
                AU  - Bulavin, Dmitry V. 
                TI  - LSEC model of aging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103492
                DO  - 10.18632/aging.103492
                SP  - 11152
                EP  - 11160
                PY  - 
                AB  - Data obtained from genetically modified mouse models suggest a detrimental role for p16High senescent cells in physiological aging and age-related pathologies. Our recent analysis of aging mice revealed a continuous and noticeable accumulation of liver sinusoid endothelial cells (LSECs) expressing numerous senescence markers, including p16. At early stage, senescent LSECs show an enhanced ability to clear macromolecular waste and toxins including oxidized LDL (oxLDL). Later in life, however, the efficiency of this important detoxifying function rapidly declines potentially due to increased endothelial thickness and senescence-induced silencing of scavenger receptors and endocytosis genes. This inability to detoxify toxins and macromolecular waste, which can be further exacerbated by increased intestinal leakiness with age, might be an important contributing factor to animal death. Here, we propose how LSEC senescence could serve as an endogenous clock that ultimately controls longevity and outline some of the possible approaches to extend the lifespan.
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Volume 12, Issue 11

About the Cover

Editorial

Michael Simons, Jeffrey R. Gulcher, Thomas W. Chittenden,

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Reviews

COVID-19 From causes of aging to death from COVID-19

Mikhail V. Blagosklonny,

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COVID-19 Potential mechanisms of hemorrhagic stroke in elderly COVID-19 patients

Haili Wang, Xiaojia Tang, Hongyang Fan, Yuhan Luo, Yuxia Song, Yao Xu, Yingzhu Chen,

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Research Perspective

COVID-19 Microdose lithium reduces cellular senescence in human astrocytes - a potential pharmacotherapy for COVID-19?

Tania Viel, Shankar Chinta, Anand Rane, Manish Chamoli, Hudson Buck, Julie Andersen,

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Priority Research Paper

Dani M. Long, Ariel K. Frame, Patrick N. Reardon, Robert C. Cumming, David A. Hendrix, Doris Kretzschmar, Jadwiga M. Giebultowicz,

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Research Papers

COVID-19 Infection with SARS-CoV-2 causes abnormal laboratory results of multiple organs in patients

Ai-Ping Yang, Hui-Ming Li, Wen-Qiang Tao, Xue-Jing Yang, Min Wang, Wen-Juan Yang, Jian-Ping Liu,

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COVID-19 Comparison of clinical characteristics and outcomes of patients with coronavirus disease 2019 at different ages

Mengmeng Zhao, Menglong Wang, Jishou Zhang, Jian Gu, Pingan Zhang, Yao Xu, Jing Ye, Zhen Wang, Di Ye, Wei Pan, Bo Shen, Hua He, Mingxiao Liu, Menglin Liu, Zhen Luo, Dan Li, Jianfang Liu, Jun Wan,

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COVID-19 ACE2 and TMPRSS2 variants and expression as candidates to sex and country differences in COVID-19 severity in Italy

Rosanna Asselta, Elvezia Maria Paraboschi, Alberto Mantovani, Stefano Duga,

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Stephanny Lizarraga, Etienne W. Daadi, Gourav Roy-Choudhury, Marcel M. Daadi,

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Jianwei Liu, Yiling Wang, Jing Guo, Jinyan Sun, Qinfeng Sun,

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Chiara Tarquini, Sabina Pucci, Maria Giovanna Scioli, Elena Doldo, Sara Agostinelli, Federico D’Amico, Alessandra Bielli, Amedeo Ferlosio, Emanuele Caredda, Umberto Tarantino, Augusto Orlandi,

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Francesca Eroli, Kristina Johnell, María Latorre Leal, Chiara Adamo, Sarah Hilmer, Jonas W. Wastesson, Angel Cedazo-Minguez, Silvia Maioli,

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Béla Ózsvári, Federica Sotgia, Michael P. Lisanti,

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Wahiba Dhahri, Sylvie Dussault, Éliane Légaré, François Rivard, Michel Desjarlais, Raphael Mathieu, Alain Rivard,

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William H. Chappell, Saverio Candido, Stephen L. Abrams, Shaw M. Akula, Linda S. Steelman, Alberto M. Martelli, Stefano Ratti, Lucio Cocco, Melchiorre Cervello, Giuseppe Montalto, Ferdinando Nicoletti, Massimo Libra, James A. McCubrey,

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Yigit Cakiroglu, Ayse Saltik, Aysen Yuceturk, Ozge Karaosmanoglu, Sule Yildirim Kopuk, Richard T. Scott Jr., Bulent Tiras, Emre Seli,

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Jun Li, Tianyu Zeng, Wei Li, Hao Wu, Chunxiao Sun, Fan Yang, Mengzhu Yang, Ziyi Fu, Yongmei Yin,

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COVID-19
From causes of aging to death from COVID-19

COVID-19
Potential mechanisms of hemorrhagic stroke in elderly COVID-19 patients

COVID-19
Microdose lithium reduces cellular senescence in human astrocytes - a potential pharmacotherapy for COVID-19?

COVID-19
Infection with SARS-CoV-2 causes abnormal laboratory results of multiple organs in patients

COVID-19
Comparison of clinical characteristics and outcomes of patients with coronavirus disease 2019 at different ages

COVID-19
ACE2 and TMPRSS2 variants and expression as candidates to sex and country differences in COVID-19 severity in Italy