Volume 12, Issue 17

Mitochondrial oxidative phosphorylation is linked to T-cell exhaustion

Shuai Jiang,

https://doi.org/10.18632/aging.103995 pp 16665—16666

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Jiang S, . Mitochondrial oxidative phosphorylation is linked to T-cell exhaustion. . 12:16665-16666. https://doi.org/10.18632/aging.103995

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The sex chromosomes of the aging epigenome

Qihua Tan,

https://doi.org/10.18632/aging.104033 pp 16667—16668

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Human skeletal stem cell aging

Thomas H. Ambrosi, L. Henry Goodnough, Charles K.F. Chan,

https://doi.org/10.18632/aging.104034 pp 16669—16671

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COVID-19
A newborn with normal IgM and elevated IgG antibodies born to an asymptomatic infection mother with COVID-19

Wenqi Gao, Zhifang Deng, Lingkong Zeng, Yuan Yang, HongJian Gong, Jue Liu, Han Xiao,

https://doi.org/10.18632/aging.103346 pp 16672—16674

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Gao W, Deng Z, Zeng L, Yang Y, Gong H, Liu J, Xiao H, . A newborn with normal IgM and elevated IgG antibodies born to an asymptomatic infection mother with COVID-19. . 12:16672-16674. https://doi.org/10.18632/aging.103346

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                TY  - JOUR
                AU  - Gao, Wenqi 
                AU  - Deng, Zhifang 
                AU  - Zeng, Lingkong 
                AU  - Yang, Yuan 
                AU  - Gong, HongJian 
                AU  - Liu, Jue 
                AU  - Xiao, Han 
                TI  - A newborn with normal IgM and elevated IgG antibodies born to an asymptomatic infection mother with COVID-19
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103346
                DO  - 10.18632/aging.103346
                SP  - 16672
                EP  - 16674
                PY  - 
                AB  - Pregnant women are susceptible population of COVID-19 which are more likely to have complications and even progress to severe illness. Pregnancy with COVID-19 and neonates are rarely reported. We report a newborn with normal IgM and elevated IgG antibodies born to an asymptomatic infection mother with COVID-19. We assessed whether there was intrauterine vertical transmission potential of COVID-19.
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COVID-19
Clinical course and risk factors for recurrence of positive SARS-CoV-2 RNA: a retrospective cohort study from Wuhan, China

Jie Chen, Xiaoping Xu, Jing Hu, Qiangda Chen, Fengfeng Xu, Hui Liang, Nanmei Liu, Hengmei Zhu, Jinlong Lan, Lan Zhou, Jiajun Xing, Ning Pu, Zhigang Cai,

https://doi.org/10.18632/aging.103795 pp 16675—16689

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Chen J, Xu X, Hu J, Chen Q, Xu F, Liang H, Liu N, Zhu H, Lan J, Zhou L, Xing J, Pu N, Cai Z, . Clinical course and risk factors for recurrence of positive SARS-CoV-2 RNA: a retrospective cohort study from Wuhan, China. . 12:16675-16689. https://doi.org/10.18632/aging.103795

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                TY  - JOUR
                AU  - Chen, Jie 
                AU  - Xu, Xiaoping 
                AU  - Hu, Jing 
                AU  - Chen, Qiangda 
                AU  - Xu, Fengfeng 
                AU  - Liang, Hui 
                AU  - Liu, Nanmei 
                AU  - Zhu, Hengmei 
                AU  - Lan, Jinlong 
                AU  - Zhou, Lan 
                AU  - Xing, Jiajun 
                AU  - Pu, Ning 
                AU  - Cai, Zhigang 
                TI  - Clinical course and risk factors for recurrence of positive SARS-CoV-2 RNA: a retrospective cohort study from Wuhan, China
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103795
                DO  - 10.18632/aging.103795
                SP  - 16675
                EP  - 16689
                PY  - 
                AB  - The coronavirus disease 2019 (COVID-19) pandemic is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The objective of this study was to determine the clinical course and risk factors for patients showing recurrent SARS-CoV-2 RNA positivity. A total of 1087 COVID-19 patients confirmed by RT-PCR from February 24, 2020 to March 31, 2020 were retrospectively enrolled. Advanced age was significantly associated with mortality. In addition, 81 (7.6%) of the discharged patients tested positive for SARS-CoV-2 RNA during the isolation period. For patients with recurrent RT-PCR positivity, the median duration from illness onset to recurrence was 50 days. Multivariate regression analysis identified elevated serum IL-6, increased lymphocyte counts and CT imaging features of lung consolidation during hospitalization as the independent risk factors of recurrence. We hypothesized that the balance between immune response and virus toxicity may be the underlying mechanism of this phenomenon. For patients with a high risk of recurrence, a prolonged observation and additional preventative measures should be implemented for at least 50 days after illness onset to prevent future outbreaks.
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Metabolic alterations in plasma from patients with familial and idiopathic Parkinson’s disease

Sokhna M.S. Yakhine-Diop, José A. Morales-García, Mireia Niso-Santano, Rosa A. González-Polo, Elisabet Uribe-Carretero, Guadalupe Martinez-Chacon, Sylvere Durand, Maria Chiara Maiuri, Ana Aiastui, Miren Zulaica, Javier Ruíz-Martínez, Adolfo López de Munain, Jordi Pérez-Tur, Ana Pérez-Castillo, Guido Kroemer, José M. Bravo-San Pedro, José M. Fuentes,

https://doi.org/10.18632/aging.103992 pp 16690—16708

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Yakhine-Diop SM, Morales-García JA, Niso-Santano M, González-Polo RA, Uribe-Carretero E, Martinez-Chacon G, Durand S, Maiuri MC, Aiastui A, Zulaica M, Ruíz-Martínez J, López de Munain A, Pérez-Tur J, et al, . Metabolic alterations in plasma from patients with familial and idiopathic Parkinson’s disease. . 12:16690-16708. https://doi.org/10.18632/aging.103992

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                TY  - JOUR
                AU  - Yakhine-Diop, Sokhna M.S. 
                AU  - Morales-García, José A. 
                AU  - Niso-Santano, Mireia 
                AU  - González-Polo, Rosa A. 
                AU  - Uribe-Carretero, Elisabet 
                AU  - Martinez-Chacon, Guadalupe 
                AU  - Durand, Sylvere 
                AU  - Maiuri, Maria Chiara 
                AU  - Aiastui, Ana 
                AU  - Zulaica, Miren 
                AU  - Ruíz-Martínez, Javier 
                AU  - López de Munain, Adolfo 
                AU  - Pérez-Tur, Jordi 
                AU  - Pérez-Castillo, Ana 
                AU  - Kroemer, Guido 
                AU  - Bravo-San Pedro, José M. 
                AU  - Fuentes, José M. 
                TI  - Metabolic alterations in plasma from patients with familial and idiopathic Parkinson’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103992
                DO  - 10.18632/aging.103992
                SP  - 16690
                EP  - 16708
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Yakhine-Diop, Sokhna M.S. 
                AU  - Morales-García, José A. 
                AU  - Niso-Santano, Mireia 
                AU  - González-Polo, Rosa A. 
                AU  - Uribe-Carretero, Elisabet 
                AU  - Martinez-Chacon, Guadalupe 
                AU  - Durand, Sylvere 
                AU  - Maiuri, Maria Chiara 
                AU  - Aiastui, Ana 
                AU  - Zulaica, Miren 
                AU  - Ruíz-Martínez, Javier 
                AU  - López de Munain, Adolfo 
                AU  - Pérez-Tur, Jordi 
                AU  - Pérez-Castillo, Ana 
                AU  - Kroemer, Guido 
                AU  - Bravo-San Pedro, José M. 
                AU  - Fuentes, José M. 
                TI  - Metabolic alterations in plasma from patients with familial and idiopathic Parkinson’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103992
                DO  - 10.18632/aging.103992
                SP  - 16690
                EP  - 16708
                PY  - 
                AB  - The research of new biomarkers for Parkinson&#x2019;s disease is essential for accurate and precocious diagnosis, as well as for the discovery of new potential disease mechanisms and drug targets. The main objective of this work was to identify metabolic changes that might serve as biomarkers for the diagnosis of this neurodegenerative disorder. For this, we profiled the plasma metabolome from mice with neurotoxin-induced Parkinson&#x2019;s disease as well as from patients with familial or sporadic Parkinson&#x2019;s disease. By using mass spectrometry technology, we analyzed the complete metabolome from healthy volunteers compared to patients with idiopathic or familial (carrying the G2019S or R1441G mutations in the LRRK2 gene) Parkinson&#x2019;s disease, as well as, from mice treated with 6-hydroxydopamine to induce Parkinson disease. Both human and murine Parkinson was accompanied by an increase in plasma levels of unconjugated bile acids (cholic acid, deoxycholic acid and lithocholic acid) and purine base intermediary metabolites, in particular hypoxanthine. The comprehensive metabolomic analysis of plasma from Parkinsonian patients underscores the importance of bile acids and purine metabolism in the pathophysiology of this disease. Therefore, plasma measurements of certain metabolites related to these pathways might contribute to the diagnosis of Parkinson&#x2019;s Disease.
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Discovering correlates of age-related decline in a healthy late-midlife male birth cohort

Kiyana Zarnani, Stephen M. Smith, Fidel Alfaro-Almagro, Birgitte Fagerlund, Martin Lauritzen, Egill Rostrup, Thomas E. Nichols,

https://doi.org/10.18632/aging.103345 pp 16709—16743

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Zarnani K, Smith SM, Alfaro-Almagro F, Fagerlund B, Lauritzen M, Rostrup E, Nichols TE, . Discovering correlates of age-related decline in a healthy late-midlife male birth cohort. . 12:16709-16743. https://doi.org/10.18632/aging.103345

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                TY  - JOUR
                AU  - Zarnani, Kiyana 
                AU  - Smith, Stephen M. 
                AU  - Alfaro-Almagro, Fidel 
                AU  - Fagerlund, Birgitte 
                AU  - Lauritzen, Martin 
                AU  - Rostrup, Egill 
                AU  - Nichols, Thomas E. 
                TI  - Discovering correlates of age-related decline in a healthy late-midlife male birth cohort
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103345
                DO  - 10.18632/aging.103345
                SP  - 16709
                EP  - 16743
                PY  - 
                AB  - Studies exploring age-related brain and cognitive change have identified substantial heterogeneity among individuals, but the underlying reasons for the differential trajectories remain largely unknown. We investigated cross-sectional and longitudinal associations between brain-imaging phenotypes (IDPs) and cognitive ability, and how these relations may be modified by common risk and protective factors. Participants were recruited from the 1953 Danish Male Birth Cohort (N=123), a longitudinal study of cognitive and brain ageing. Childhood IQ and socio-demographic factors are available for these participants who have been assessed regularly on multiple IDPs and behavioural factors in midlife. Using Pearson correlations and canonical correlation analysis (CCA), we explored the relation between 454 IDPs and 114 behavioural variables. CCA identified a single mode of population covariation coupling cross-subject longitudinal changes in brain structure to changes in cognitive performance and to a range of age-related covariates (r=0.92, Pcorrected &lt; 0.001). Specifically, this CCA-mode indicated that; decreases in IQ and speed assessed tasks, higher rates of familial myocardial infarct, less physical activity, and poorer mental health are associated with larger decreases in whole brain grey matter and white matter. We found no evidence supporting the role of baseline scores as predictors of impending brain and behavioural change in late-midlife.
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Cancer mortality in the oldest old: a global overview

Dana Hashim, Greta Carioli, Matteo Malvezzi, Paola Bertuccio, Samuel Waxman, Eva Negri, Carlo La Vecchia, Paolo Boffetta,

https://doi.org/10.18632/aging.103503 pp 16744—16758

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Hashim D, Carioli G, Malvezzi M, Bertuccio P, Waxman S, Negri E, La Vecchia C, Boffetta P, . Cancer mortality in the oldest old: a global overview. . 12:16744-16758. https://doi.org/10.18632/aging.103503

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                TY  - JOUR
                AU  - Hashim, Dana 
                AU  - Carioli, Greta 
                AU  - Malvezzi, Matteo 
                AU  - Bertuccio, Paola 
                AU  - Waxman, Samuel 
                AU  - Negri, Eva 
                AU  - La Vecchia, Carlo 
                AU  - Boffetta, Paolo 
                TI  - Cancer mortality in the oldest old: a global overview
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103503
                DO  - 10.18632/aging.103503
                SP  - 16744
                EP  - 16758
                PY  - 
                AB  - Background: As a higher proportion of adults live beyond 85 years, their cancer burden is expected to increase. While trends among the oldest old are established for major epithelial cancers (breast, prostate, lung, and colorectal cancers), they are less studied for minor cancers. This study describes age trends of cancer mortality, with emphasis on individuals aged 85+ years.Results: Overall cancer mortality peaked at 85 years old and decreased or stabilized for all countries except the USA, France, and Japan, in which mortality continued to increase after age 85 years. For most countries, cancers of the oesophagus, stomach, liver, and larynx have a similar flat trend patterns across all ages. Bladder and kidney cancers as well as non-Hodgkin lymphoma, multiple myeloma, and leukemia showed a decreasing pattern after 85 years for UK, Germany, Italy and Poland. Lung cancer peaked at 80 years, although the age-specific peak among women did not follow the same pattern among all countries. Breast and prostate cancers increased after 85 years.Conclusion: Mortality stabilized or decreased after age 85, particularly for non-hormonal cancers. Whether this reflects a true biological levelling of mortality rates, or lower validity of cancer registration among the oldest old, remains open to discussion.Methods: Completed death data were obtained from the World Health Organization (WHO) for eight countries (2000 to 2014). Age-specific mortality rates were calculated for each 5-year age group above age 64. Joinpoint regression models were used to identify significant changes in mortality trends by age.
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HDAC4 inhibition disrupts TET2 function in high-risk MDS and AML

Feiteng Huang, Jie Sun, Wei Chen, Xin He, Yinghui Zhu, Haojie Dong, Hanying Wang, Zheng Li, Lei Zhang, Samer Khaled, Guido Marcucci, Jinwen Huang, Ling Li,

https://doi.org/10.18632/aging.103605 pp 16759—16774

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Huang F, Sun J, Chen W, He X, Zhu Y, Dong H, Wang H, Li Z, Zhang L, Khaled S, Marcucci G, Huang J, Li L, . HDAC4 inhibition disrupts TET2 function in high-risk MDS and AML. . 12:16759-16774. https://doi.org/10.18632/aging.103605

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                TY  - JOUR
                AU  - Huang, Feiteng 
                AU  - Sun, Jie 
                AU  - Chen, Wei 
                AU  - He, Xin 
                AU  - Zhu, Yinghui 
                AU  - Dong, Haojie 
                AU  - Wang, Hanying 
                AU  - Li, Zheng 
                AU  - Zhang, Lei 
                AU  - Khaled, Samer 
                AU  - Marcucci, Guido 
                AU  - Huang, Jinwen 
                AU  - Li, Ling 
                TI  - HDAC4 inhibition disrupts TET2 function in high-risk MDS and AML
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103605
                DO  - 10.18632/aging.103605
                SP  - 16759
                EP  - 16774
                PY  - 
                AB  - Aberrant DNA methylation often silences transcription of tumor-suppressor genes and is considered a hallmark of myeloid neoplasms. Similarly, histone deacetylation represses transcription of genes responsible for cell differentiation/death. A previous clinical study suggested potential pharmacodynamic antagonism between histone deacetylase inhibitors (HDACi) and DNA hypomethylating agents (HMA). Herein, to determine such antagonism, we used MDS/AML lines and NHD13 transgenic mice, and demonstrated that treatment with the pan-HDACi suberoylanilide hydroxamic acid (SAHA) significantly decreased TET2 expression and global 5-hydroxymethylcytosine (5hmC) levels. Mechanistically, our RNAi screen revealed that HDAC4 was responsible for maintaining TET2 levels. Accordingly, HDAC4 knockout reduced expression levels of MTSS1, a known TET2 target, an event associated with decreased 5hmC enrichment on the MTSS1 enhancer. Retrospective analysis of GEO datasets demonstrated that lower HDAC4 levels predict worse prognosis for AML patients. In an MDS-L xenografted immunodeficient mouse model, vitamin C co-treatment prevented TET2 loss of activity seen following SAHA treatment. Accordingly, vitamin C co-treatment further reduced MDS-L cell engraftment relative to SAHA alone. In summary, our findings suggest that co-administration of a TET2 agonist with pan-HDACi treatment could effectively counter potential diminution in TET2 activity resulting from pan-HDACi treatment alone, providing a rationale for evaluating such combinations against high-risk MDS/AML.
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Identification of cardiovascular health gene variants related to longevity in a Chinese population

Li Zhang, Chen Bai, Chao Nie, Xiaoquan Zhu, Huiping Yuan, Liang Sun, Qi Zhou, Xiaoling Li, Xuan Xian, Fan Yang, Guofang Pang, Yuan Lv, Xiaolin Ni, Caiyou Hu, Ze Yang,

https://doi.org/10.18632/aging.103396 pp 16775—16802

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Zhang L, Bai C, Nie C, Zhu X, Yuan H, Sun L, Zhou Q, Li X, Xian X, Yang F, Pang G, Lv Y, Ni X, et al, . Identification of cardiovascular health gene variants related to longevity in a Chinese population. . 12:16775-16802. https://doi.org/10.18632/aging.103396

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                TY  - JOUR
                AU  - Zhang, Li 
                AU  - Bai, Chen 
                AU  - Nie, Chao 
                AU  - Zhu, Xiaoquan 
                AU  - Yuan, Huiping 
                AU  - Sun, Liang 
                AU  - Zhou, Qi 
                AU  - Li, Xiaoling 
                AU  - Xian, Xuan 
                AU  - Yang, Fan 
                AU  - Pang, Guofang 
                AU  - Lv, Yuan 
                AU  - Ni, Xiaolin 
                AU  - Hu, Caiyou 
                AU  - Yang, Ze 
                TI  - Identification of cardiovascular health gene variants related to longevity in a Chinese population
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103396
                DO  - 10.18632/aging.103396
                SP  - 16775
                EP  - 16802
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Zhang, Li 
                AU  - Bai, Chen 
                AU  - Nie, Chao 
                AU  - Zhu, Xiaoquan 
                AU  - Yuan, Huiping 
                AU  - Sun, Liang 
                AU  - Zhou, Qi 
                AU  - Li, Xiaoling 
                AU  - Xian, Xuan 
                AU  - Yang, Fan 
                AU  - Pang, Guofang 
                AU  - Lv, Yuan 
                AU  - Ni, Xiaolin 
                AU  - Hu, Caiyou 
                AU  - Yang, Ze 
                TI  - Identification of cardiovascular health gene variants related to longevity in a Chinese population
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103396
                DO  - 10.18632/aging.103396
                SP  - 16775
                EP  - 16802
                PY  - 
                AB  - Cardiovascular disease (CVD) is one of the most important causes of human death, but no attention has been paid to cardiovascular health genes related to healthy longevity. Therefore, we developed a cohort study to explore such genes in healthy, long-lived Chinese subjects. A total of 13275 healthy elderly people were enrolled, including 5107 healthy long-lived individuals and 8168 age-matched control individuals with low CVD risk. Using a combination of whole-exome sequencing (WES) and genome-wide association studies (GWAS), we identified 2 genetic variants (TFPI rs7586970 T, p=0.013, OR=1.100. ADAMTS7 rs3825807 A, p=0.017, OR=1.198) associated with healthy lipid metabolism and longevity. Furthermore, we showed that an interaction among TFPI rs7586970, ADAMTS7 rs3825807 and APOE &#x25B;3 maintained normal blood lipid levels in centenarians by stratified analysis of CVD risk factors. Finally, through biological function analysis, we revealed clues regarding the mechanism of factor related to cardiovascular health (FCH) such as lipids and longevity. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that the two variants above may be associated with longevity via FCH lipid metabolism pathways. From a meta-analysis of venous thrombosis patients, we unexpectedly found that rs7586970 T is associated with both longevity and protection against vascular disease.
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Anchorage independence altered vasculogenic phenotype of melanoma cells through downregulation in aminopeptidase N /syndecan-1/integrin β4 axis

Yu-Che Cheng, Wei-Chi Ku, Ting-Ting Tseng, Ching-Po Wu, Mengjin Li, Shao-Chen Lee,

https://doi.org/10.18632/aging.103425 pp 16803—16819

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Cheng Y, Ku W, Tseng T, Wu C, Li M, Lee S, . Anchorage independence altered vasculogenic phenotype of melanoma cells through downregulation in aminopeptidase N /syndecan-1/integrin β4 axis. . 12:16803-16819. https://doi.org/10.18632/aging.103425

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                TY  - JOUR
                AU  - Cheng, Yu-Che 
                AU  - Ku, Wei-Chi 
                AU  - Tseng, Ting-Ting 
                AU  - Wu, Ching-Po 
                AU  - Li, Mengjin 
                AU  - Lee, Shao-Chen 
                TI  - Anchorage independence altered vasculogenic phenotype of melanoma cells through downregulation in aminopeptidase N /syndecan-1/integrin β4 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103425
                DO  - 10.18632/aging.103425
                SP  - 16803
                EP  - 16819
                PY  - 
                AB  - The detachment of tumor cells from extracellular matrix and survival under anchorage-independence were recognized as the initial step of tumor metastasis. Previously we had demonstrated that anchorage-independence altered gene expressions and showed characteristics of cell invasiveness loss, enhanced chemosensitivity, and enhanced subcutaneous tumor formation. However, whether it affected histological phenotypes in tumor tissues remained unclear.
                Melanoma metastases were generated in nude mice using adherent or suspended melanoma cells. Examination of melanoma metastases revealed histological features of extensive vascular structures in adherent cell-derived tumors, while not seen in suspended cell-derived tumors. Quantitative proteomic analysis at adherent, suspended, and re-attached melanoma cells suggested that aminopeptidase N was potentially downregulated upon cell suspension or reattachment. Downregulation of aminopeptidase N by gene-specific shRNAs showed reduced cell invasiveness and enhanced subcutaneous tumor formation that was consistent with previous observations. Experiments by suppression or overexpression of aminopeptidase N expression demonstrated that aminopeptidase N regulated syndecan-1 and integrin &#x3B2;4 expression through PKC&#x3B4; pathway. Histological analysis at melanoma metastases further suggested that CD31+/aminopeptidase N+/syndecan-1+/integrin &#x3B2;4+ phenotypes were associated with vascular structures.
                In summary, we suggested the expression axis of aminopeptidase N/syndecan-1/integrin &#x3B2;4 in melanoma cells was suppressed by detachment stress, which diminished vascular phenotypes of melanoma metastases.
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Neutrophil extracellular traps amplify neutrophil recruitment and inflammation in neutrophilic asthma by stimulating the airway epithelial cells to activate the TLR4/ NF-κB pathway and secrete chemokines

Rongjun Wan, Juan Jiang, Chengping Hu, Xi Chen, Cen Chen, Bingrong Zhao, Xinyue Hu, Zhiyuan Zheng, Yuanyuan Li,

https://doi.org/10.18632/aging.103479 pp 16820—16836

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Wan R, Jiang J, Hu C, Chen X, Chen C, Zhao B, Hu X, Zheng Z, Li Y, . Neutrophil extracellular traps amplify neutrophil recruitment and inflammation in neutrophilic asthma by stimulating the airway epithelial cells to activate the TLR4/ NF-κB pathway and secrete chemokines. . 12:16820-16836. https://doi.org/10.18632/aging.103479

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                TY  - JOUR
                AU  - Wan, Rongjun 
                AU  - Jiang, Juan 
                AU  - Hu, Chengping 
                AU  - Chen, Xi 
                AU  - Chen, Cen 
                AU  - Zhao, Bingrong 
                AU  - Hu, Xinyue 
                AU  - Zheng, Zhiyuan 
                AU  - Li, Yuanyuan 
                TI  - Neutrophil extracellular traps amplify neutrophil recruitment and inflammation in neutrophilic asthma by stimulating the airway epithelial cells to activate the TLR4/ NF-κB pathway and secrete chemokines
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103479
                DO  - 10.18632/aging.103479
                SP  - 16820
                EP  - 16836
                PY  - 
                AB  - Neutrophilic asthma (NA) is a distinct airway inflammation disease with prominent neutrophil infiltration. The role played by neutrophil extracellular traps (NETs) in NA, however, is quite unclear. This study was based on the hypothesis that NETs are responsible for the second neutrophil wave and therefore contribute significantly to inflammation. The proinflammatory effects of NETs were evaluated in vitro and in vivo. Formation of NETs and neutrophil swarming was seen in a mouse model of NA. Additionally, NETs were found to stimulate airway cells to express CXCL1, CXCL2, and CXCL8 via the TLR4/NF-&#x3BA;B pathway, which recruits neutrophils to the inflammation site. Furthermore, prevention of NET formation decreased the recruitment of lung neutrophils and hence reduce neutrophilic inflammation. Additionally, the structural integrity of NETs had no effect on the recruitment of lung neutrophils and neutrophilic inflammation. In NA mice, NETs could trigger airway and alveolar epithelial cells to express chemokines which recruit more neutrophils via activation of the TLR4/NF-&#x3BA;B pathway.
                ER  -

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Sulforaphane-cysteine downregulates CDK4 /CDK6 and inhibits tubulin polymerization contributing to cell cycle arrest and apoptosis in human glioblastoma cells

Juntao Li, Yan Zhou, Yuting Yan, Zhongnan Zheng, Yabin Hu, Wei Wu,

https://doi.org/10.18632/aging.103537 pp 16837—16851

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Li J, Zhou Y, Yan Y, Zheng Z, Hu Y, Wu W, . Sulforaphane-cysteine downregulates CDK4 /CDK6 and inhibits tubulin polymerization contributing to cell cycle arrest and apoptosis in human glioblastoma cells. . 12:16837-16851. https://doi.org/10.18632/aging.103537

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                TY  - JOUR
                AU  - Li, Juntao 
                AU  - Zhou, Yan 
                AU  - Yan, Yuting 
                AU  - Zheng, Zhongnan 
                AU  - Hu, Yabin 
                AU  - Wu, Wei 
                TI  - Sulforaphane-cysteine downregulates CDK4 /CDK6 and inhibits tubulin polymerization contributing to cell cycle arrest and apoptosis in human glioblastoma cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103537
                DO  - 10.18632/aging.103537
                SP  - 16837
                EP  - 16851
                PY  - 
                AB  - Here we demonstrated that sulforaphane-cysteine (SFN-Cys) regulated cell cycle-related protein expressions in G0/G1 and G2/M phases of U87MG cells via High Performance Liquid Chromatography-Mass Spectrometry/Mass Spectrometry (HPLC-MS/MS) and proteomics analysis. Further, mRNA products of CDK4, CDK6 and &#x3B1;-tubulin were significantly higher in glioblastoma than those in normal tissues, and these results were significantly correlated to pathological grades and clinical prognosis via analyzing TCGA and CGGA databases. Furthermore, Western blot showed that SFN-Cys downregulated CDK4, CDK6 and p-Rb in a dose-dependent manner and these results were reversed by p-ERK1/2 blocker PD98059 in U87MG and U373MG cells. The reductions of CDK4, CDK6 and p-Rb were reversed by proteasome inhibitor MG132; similarly, the upregulation of 26S proteasome by SFN-Cys was reversed by PD98059. Interestingly, SFN-Cys decreased CDK4 and CDK6 by phosphorylated ERK1/2-caused proteasomal degradation resulting in decreased Rb phosphorylation contributing to cell cycle arrest in G0/G1 phase. Besides, Western blot showed that SFN-Cys downregulated &#x3B1;-tubulin resulting in microtubule disruption and aggregation, and cell cycle arrest in G2/M phase and apoptosis. These results might help us understand the molecular etiology of glioblastoma progression to establish brand-new anti-cancer therapies.
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Spermidine inhibits neurodegeneration and delays aging via the PINK1-PDR1-dependent mitophagy pathway in C. elegans

Xin Yang, Mohan Zhang, Yuhua Dai, Yuchao Sun, Yahyah Aman, Yuying Xu, Peilin Yu, Yifan Zheng, Jun Yang, Xinqiang Zhu,

https://doi.org/10.18632/aging.103578 pp 16852—16866

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Yang X, Zhang M, Dai Y, Sun Y, Aman Y, Xu Y, Yu P, Zheng Y, Yang J, Zhu X, . Spermidine inhibits neurodegeneration and delays aging via the PINK1-PDR1-dependent mitophagy pathway in C. elegans. . 12:16852-16866. https://doi.org/10.18632/aging.103578

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Provider: 
 TY - JOUR
 AU - Yang, Xin 
 AU - Zhang, Mohan 
 AU - Dai, Yuhua 
 AU - Sun, Yuchao 
 AU - Aman, Yahyah 
 AU - Xu, Yuying 
 AU - Yu, Peilin 
 AU - Zheng, Yifan 
 AU - Yang, Jun 
 AU - Zhu, Xinqiang 
 TI - Spermidine inhibits neurodegeneration and delays aging via the PINK1-PDR1-dependent mitophagy pathway in C. elegans
 JO - 
 JA - 
 VL - 12
 IS - 17
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103578
 DO - 10.18632/aging.103578
 SP - 16852
 EP - 16866
 PY - 
 AB - Aging is the primary driver of various diseases, including common neurodegenerative diseases such as Alzheimer&#x2019;s disease (AD) and Parkinson&#x2019;s disease (PD). Currently there is no cure for AD and PD, and the development of novel drug candidates is demanding. Spermidine is a small anti-aging molecule with elimination of damaged mitochondria via the process of mitophagy identified as a molecular mechanism of action. Here, we show that spermidine inhibits memory loss in AD worms and improves behavioral performance, e.g., locomotor capacity, in a PD worm model, both via the PINK1-PDR1-dependent mitophagy pathway. Additionally, spermidine delays accelerated aging and improves healthspan in the DNA repair-deficient premature aging Werner syndrome (WS) worm model. While possible intertwined interactions between mitophagy/autophagy induction and DNA repair by spermidine are to be determined, our data support further translation of spermidine as a possible therapeutic intervention for such diseases.
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Oxidative stress, apoptosis and inflammatory responses involved in copper-induced pulmonary toxicity in mice

Zhijie Jian, Hongrui Guo, Huan Liu, Hengmin Cui, Jing Fang, Zhicai Zuo, Junliang Deng, Yinglun Li, Xun Wang, Ling Zhao,

https://doi.org/10.18632/aging.103585 pp 16867—16886

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Jian Z, Guo H, Liu H, Cui H, Fang J, Zuo Z, Deng J, Li Y, Wang X, Zhao L, . Oxidative stress, apoptosis and inflammatory responses involved in copper-induced pulmonary toxicity in mice. . 12:16867-16886. https://doi.org/10.18632/aging.103585

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                TY  - JOUR
                AU  - Jian, Zhijie 
                AU  - Guo, Hongrui 
                AU  - Liu, Huan 
                AU  - Cui, Hengmin 
                AU  - Fang, Jing 
                AU  - Zuo, Zhicai 
                AU  - Deng, Junliang 
                AU  - Li, Yinglun 
                AU  - Wang, Xun 
                AU  - Zhao, Ling 
                TI  - Oxidative stress, apoptosis and inflammatory responses involved in copper-induced pulmonary toxicity in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103585
                DO  - 10.18632/aging.103585
                SP  - 16867
                EP  - 16886
                PY  - 
                AB  - At present, there are few studies focused on the relationship between copper (Cu) and oxidative stress, apoptosis, or inflammatory responses in animal and human lungs. This study was conducted to explore the effects of Cu on pulmonary oxidative stress, apoptosis and inflammatory responses in mice orally administered with 0 mg/kg (control), 10 mg/kg, 20 mg/kg, and 40 mg/kg of CuSO4 for 42 days. The results showed that CuSO4 increased ROS production, and MDA, 8-OHdG and NO contents as well as iNOS activities and mRNA expression levels. Meanwhile, CuSO4 reduced the activities and mRNA expression levels of antioxidant enzymes (GSH-Px, CAT, and SOD) and GSH contents, and ASA and AHR abilities. Also, CuSO4 induced apoptosis, which was accompanied by decreasing Bcl-2, Bcl-xL mRNA expression levels and protein expression levels, and increasing Bax, Bak, cleaved-caspase-3, cleaved-caspase-9 mRNA, and protein expression levels, and Bax/Bcl-2 ratio. Concurrently, CuSO4 caused inflammation by increasing MPO activities and activating the NF-&#x3BA;B signalling pathway, and down-regulating the mRNA and protein expression levels of anti-inflammatory cytokines (IL-2, IL-4, IL-10). In conclusion, the abovementioned findings demonstrated that over 10 mg/kg CuSO4 can cause oxidative stress, apoptosis, and inflammatory responses, which contribute to pulmonary lesions and dysfunction in mice.
                ER  -

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Celastrol regulates bone marrow mesenchymal stem cell fate and bone-fat balance in osteoporosis and skeletal aging by inducing PGC-1α signaling

Li Li, Bing Wang, Yawei Li, Lei Li, Yuliang Dai, Guohua Lv, Pengfei Wu, Pengzhi Li,

https://doi.org/10.18632/aging.103590 pp 16887—16898

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Li L, Wang B, Li Y, Li L, Dai Y, Lv G, Wu P, Li P, . Celastrol regulates bone marrow mesenchymal stem cell fate and bone-fat balance in osteoporosis and skeletal aging by inducing PGC-1α signaling. . 12:16887-16898. https://doi.org/10.18632/aging.103590

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                TY  - JOUR
                AU  - Li, Li 
                AU  - Wang, Bing 
                AU  - Li, Yawei 
                AU  - Li, Lei 
                AU  - Dai, Yuliang 
                AU  - Lv, Guohua 
                AU  - Wu, Pengfei 
                AU  - Li, Pengzhi 
                TI  - Celastrol regulates bone marrow mesenchymal stem cell fate and bone-fat balance in osteoporosis and skeletal aging by inducing PGC-1α signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103590
                DO  - 10.18632/aging.103590
                SP  - 16887
                EP  - 16898
                PY  - 
                AB  - Celastrol has recently been identified as a prospective new treatment for obesity and several metabolic complications. However, the effect of Celastrol in osteoporosis (OP) remains unknown. In this study, we demonstrated that Celastrol promotes osteoblast differentiation and prevents adipocyte differentiation in bone marrow mesenchymal stem cells (BM-MSCs) in vitro. Mechanistically, Celastrol was able to control the differentiation of BM-MSCs by stimulating PGC-1&#x3B1; signaling. Moreover, administration of Celastrol could alleviate bone loss and bone marrow adipose tissue (MAT) accumulation in ovariectomized (OVX) mice and aged mice. Together, these results recommended that Celastrol could regulate BM-MSCs fate and bone-fat balance in OP and skeletal aging by stimulating PGC-1&#x3B1;, which might act as a possible therapeutic target for OP and for the prevention of skeletal aging.
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Umbilical cord mesenchymal stem cells protect thymus structure and function in aged C57 mice by downregulating aging-related genes and upregulating autophagy- and anti-oxidative stress-related genes

Xing-Hua Pan, Qing-Keng Lin, Xiang Yao, Zi-An Li, Xue-Min Cai, Rong-Qing Pang, Guang-Ping Ruan,

https://doi.org/10.18632/aging.103594 pp 16899—16920

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Pan X, Lin Q, Yao X, Li Z, Cai X, Pang R, Ruan G, . Umbilical cord mesenchymal stem cells protect thymus structure and function in aged C57 mice by downregulating aging-related genes and upregulating autophagy- and anti-oxidative stress-related genes. . 12:16899-16920. https://doi.org/10.18632/aging.103594

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                TY  - JOUR
                AU  - Pan, Xing-Hua 
                AU  - Lin, Qing-Keng 
                AU  - Yao, Xiang 
                AU  - Li, Zi-An 
                AU  - Cai, Xue-Min 
                AU  - Pang, Rong-Qing 
                AU  - Ruan, Guang-Ping 
                TI  - Umbilical cord mesenchymal stem cells protect thymus structure and function in aged C57 mice by downregulating aging-related genes and upregulating autophagy- and anti-oxidative stress-related genes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103594
                DO  - 10.18632/aging.103594
                SP  - 16899
                EP  - 16920
                PY  - 
                AB  - Background: To study the effect of allogeneic umbilical cord mesenchymal stem cell transplantation on the structure and function of the thymus in aged C57 mice and provide a new method for the treatment of senile thymic atrophy.
                Results: The changes in the thymus cortex and medulla volume and the lymphocyte ratio were analyzed by immunofluorescence. For thymus tissue sections, immunohistochemical staining was performed to detect p16, p53, SOD, becline1, LC3b, p62, sirt1, and sirt3. Changes in CK5, CK8, CD4 and CD8 expression were observed. Treatment with mUCMSCs could promote hair regeneration in aging mice and regenerate the thymus structure.
                Conclusions: mUCMSCs inhibited senescence of the thymus and promoted structural and functional thymus regeneration by downregulating the senescence genes p53 and p16 and upregulating the SOD, Sirt1 and Sirt3 genes, but the mechanism requires further research.
                Methods: C57 mice were obtained and met the requirements of thymic aging. mUCMSCs were infused via the tail vein at a dose of 1&#xD7;107 cells/kg twice per week for 3 weeks. Six weeks after the last transplantation, the thymus was weighed, and the thymus-to-body weight ratio was calculated. The thymus tissue was stained with HE.
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Epigenetic upregulation of HOXC10 in non-small lung cancer cells

Miao Li, John Simon Alsager, Zhaokai Wang, Lin Cheng, Bin Shan,

https://doi.org/10.18632/aging.103597 pp 16921—16935

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Li M, Alsager JS, Wang Z, Cheng L, Shan B, . Epigenetic upregulation of HOXC10 in non-small lung cancer cells. . 12:16921-16935. https://doi.org/10.18632/aging.103597

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Provider: 
 TY - JOUR
 AU - Li, Miao 
 AU - Alsager, John Simon 
 AU - Wang, Zhaokai 
 AU - Cheng, Lin 
 AU - Shan, Bin 
 TI - Epigenetic upregulation of HOXC10 in non-small lung cancer cells
 JO - 
 JA - 
 VL - 12
 IS - 17
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103597
 DO - 10.18632/aging.103597
 SP - 16921
 EP - 16935
 PY - 
 AB - The homeobox genes (HOX) have emerged as a new family of master regulators of development and cancer. In the current study, we examined the expression and function of HOXC10 in human non-small cell lung cancer (NSCLC). We observed increased expression of HOXC10 in the more aggressive human NSCLC cell line NCI-H23 over the well differentiated A549 cells. To elucidate the expression and function of HOXC10 in NSCLC cells, we employed RT-PCR, immunoblotting, methylation-specific PCR, apoptosis assays, and xenograft model. Overexpression of HOXC10 in A549 cells conveyed increased proliferation, reduced apoptosis, and accelerated tumor growth when transplanted into nude mice. In contrast, siRNA-mediated knockdown of HOXC10 in NCI-H23 cells reduced proliferation and increased apoptosis. Our results further indicated that hypomethylation of the CpG island in the HOXC10 promoter was critical to elevated expression of HOXC10 in NSCLC cells. Lastly, we identified a G-quadruplex in the HOXC10 promoter and its G-quadruplex formation was required for elevated expression of HOXC10 in NSCLC cells. Moreover our results suggest that disruption of G-quadruplex formation can silence HOXC10 expression in NSCLC cells. In summary, we report HOXC10 as a novel tumor promoting oncogene in NSCLC cells.
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Long non-coding RNA FAM133B-2 represses the radio-resistance of nasopharyngeal cancer cells by targeting miR-34a-5p/CDK6 axis

Dabing Huang, Xianhai Zhu, Yong Wang, Haobin Yu, Youguang Pu,

https://doi.org/10.18632/aging.103600 pp 16936—16950

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Huang D, Zhu X, Wang Y, Yu H, Pu Y, . Long non-coding RNA FAM133B-2 represses the radio-resistance of nasopharyngeal cancer cells by targeting miR-34a-5p/CDK6 axis. . 12:16936-16950. https://doi.org/10.18632/aging.103600

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                TY  - JOUR
                AU  - Huang, Dabing 
                AU  - Zhu, Xianhai 
                AU  - Wang, Yong 
                AU  - Yu, Haobin 
                AU  - Pu, Youguang 
                TI  - Long non-coding RNA FAM133B-2 represses the radio-resistance of nasopharyngeal cancer cells by targeting miR-34a-5p/CDK6 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103600
                DO  - 10.18632/aging.103600
                SP  - 16936
                EP  - 16950
                PY  - 
                AB  - Long non-coding RNAs (lncRNAs) were found to play roles in various cancers, including nasopharyngeal carcinoma. In this study, we focused on the biological function of the lncRNA FAM133B-2 in the radio-resistance of nasopharyngeal carcinoma. The RNA-seq and qRT-PCR analysis showed that FAM133B-2 is highly expressed in the radio-resistant nasopharyngeal carcinoma cells. The following biochemical assays showed that FAM133B-2 represses the nasopharyngeal carcinoma radio-resistance and also affects the apoptosis and proliferation of nasopharyngeal carcinoma cells. Further investigations suggested that miR-34a-5p targets FAM133B-2 and also regulates the cyclin-dependent kinase 6 (CDK6). All these results suggested that the lncRNA FAM133B-2 might function as a competitive endogenous RNA (ceRNA) for miR-34a-5p in nasopharyngeal carcinoma radio-resistance, thus it may be regarded as a novel prognostic biomarker and therapeutic target in nasopharyngeal carcinoma diagnosis and treatment.
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Esculentoside A rescues granulosa cell apoptosis and folliculogenesis in mice with premature ovarian failure

Zhenteng Liu, Fenghua Li, Jingwen Xue, Meimei Wang, Shoucui Lai, Hongchu Bao, Shunzhi He,

https://doi.org/10.18632/aging.103609 pp 16951—16962

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Liu Z, Li F, Xue J, Wang M, Lai S, Bao H, He S, . Esculentoside A rescues granulosa cell apoptosis and folliculogenesis in mice with premature ovarian failure. . 12:16951-16962. https://doi.org/10.18632/aging.103609

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                TY  - JOUR
                AU  - Liu, Zhenteng 
                AU  - Li, Fenghua 
                AU  - Xue, Jingwen 
                AU  - Wang, Meimei 
                AU  - Lai, Shoucui 
                AU  - Bao, Hongchu 
                AU  - He, Shunzhi 
                TI  - Esculentoside A rescues granulosa cell apoptosis and folliculogenesis in mice with premature ovarian failure
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103609
                DO  - 10.18632/aging.103609
                SP  - 16951
                EP  - 16962
                PY  - 
                AB  - Follicular atresia is one of the main processes for the loss of granulosa cells and oocytes from the mammalian ovary and any impairment to premature ovarian failure. Large numbers of studies have demonstrated that granulosa cell apoptosis causes follicular atresia, yet the rescue of these cells remains elusive. We aimed to use Esculentoside A (3-O-b-D-glucopyranosyl-1, 4-b-D-xylopyranosyl) phytolaccagenin, a saponin extracted from Phytolacca esculenta roots, as a potential rescue agent for the apoptosis of granulosa cells. Our results revealed the rescue of normal body and ovary weights, normal ovarian histo-architecture of ovaries, and hormones levels with regular estrus cycle. Consistently, the expression of proliferating and anti-apoptotic markers, i.e. KI67 and BCL-2 in granulosa cells, was enhanced. Meanwhile, the expressions of pro-apoptotic markers, which were BAX and CASPASEs (CASPASE-9 and CASPASE-3), were prominently reduced in Esculentoside A-induced premature ovarian failure mice. Additionally, PPAR&#x3B3;, a potential therapeutic target, has also rescued its expression by treating the premature ovarian failure mice with Esculentoside A. Our results advocated that Esculentoside A could restore folliculogenesis in premature ovarian failure mice. Furthermore, it has the potential to be investigated as a therapeutic agent for premature ovarian failure.
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PGC-1α and ERRα in patients with endometrial cancer: a translational study for predicting myometrial invasion

LiLi Chen, XiaoDan Mao, MeiMei Huang, HuiFang Lei, LiFang Xue, PengMing Sun,

https://doi.org/10.18632/aging.103611 pp 16963—16980

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Chen L, Mao X, Huang M, Lei H, Xue L, Sun P, . PGC-1α and ERRα in patients with endometrial cancer: a translational study for predicting myometrial invasion. . 12:16963-16980. https://doi.org/10.18632/aging.103611

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                TY  - JOUR
                AU  - Chen, LiLi 
                AU  - Mao, XiaoDan 
                AU  - Huang, MeiMei 
                AU  - Lei, HuiFang 
                AU  - Xue, LiFang 
                AU  - Sun, PengMing 
                TI  - PGC-1α and ERRα in patients with endometrial cancer: a translational study for predicting myometrial invasion
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103611
                DO  - 10.18632/aging.103611
                SP  - 16963
                EP  - 16980
                PY  - 
                AB  - Background: PGC-1&#x3B1; and ERR&#x3B1; are closely related to tumor formation and progression. However, the mechanism underlying the involvement of PGC-1&#x3B1;/ERR&#x3B1; in regulating invasion and migration in endometrial cancer remains to be explored.Results: Elevated levels of PGC-1&#x3B1; and ERR&#x3B1; were associated with advanced myometrial invasion, and PGC-1&#x3B1; and Vimentin expression was related to the depth of myometrial invasion in premenopausal endometrial cancer. Silencing of PGC-1&#x3B1; reduced ERR&#x3B1; activation and inhibited epithelial-mesenchymal-transition phenotypes, resulting in significant inhibition of invasion and migration. Overexpression of ERR&#x3B1; led to enhanced PGC-1&#x3B1; expression and increased activity of TFEB, promoting epithelial-mesenchymal-transition in endometrial cancer cells.Conclusions: PGC-1&#x3B1; and ERR&#x3B1; induce the epithelial-mesenchymal-transition therefore invasion and migration in endometrial cancer, and may be novel biomarkers to predict the risk of advanced myometrial invasion.Methods: PGC-1&#x3B1;, ERR&#x3B1;, and vimentin expression was analyzed in tissue microarrays using immunohistochemistry. PGC-1&#x3B1; and ERR&#x3B1; expression in endometrial cancer cell lines was investigated using quantitative PCR and western blotting analyses after infection with lentivirus-mediated small interfering RNA (siRNA) targeting PGC-1&#x3B1; (siRNA-PGC-1&#x3B1;) or overexpressing ERR&#x3B1;. E-cadherin and vimentin levels were determined using western blotting and cell immunouorescence analyses. Cell migration and invasiveness were evaluated using scratch and trans-well chamber assays.
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Annotation of susceptibility SNPs associated with atrial fibrillation

Chengqi Xu, Rongfeng Zhang, Yunlong Xia, Liang Xiong, Wei Yang, Pengyun Wang,

https://doi.org/10.18632/aging.103615 pp 16981—16998

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Xu C, Zhang R, Xia Y, Xiong L, Yang W, Wang P, . Annotation of susceptibility SNPs associated with atrial fibrillation. . 12:16981-16998. https://doi.org/10.18632/aging.103615

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                TY  - JOUR
                AU  - Xu, Chengqi 
                AU  - Zhang, Rongfeng 
                AU  - Xia, Yunlong 
                AU  - Xiong, Liang 
                AU  - Yang, Wei 
                AU  - Wang, Pengyun 
                TI  - Annotation of susceptibility SNPs associated with atrial fibrillation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103615
                DO  - 10.18632/aging.103615
                SP  - 16981
                EP  - 16998
                PY  - 
                AB  - Objective: Genome-wide association studies (GWAS) and the candidate gene based association studies have identified a panel of variants associated with atrial fibrillation (AF), however, most of the identified single nucleotide polymorphisms (SNPs) were found located within intergenic or intronic genomic regions, and whether the positive SNPs have a real biological function is unknown, and the real disease causing gene need to be studied.
                Results: The current results of the genetic studies including common variants identified by GWAS (338 index SNPs) and candidate gene based association studies (40 SNPs) were summarized.
                Conclusion: Our study suggests the relationship between genetic variants and possible targeted genes, and provides insight into potential genetic pathways underlying AF incidence and development. The results may provide an encyclopedia of AF susceptibility SNPs and shed light on the functional mechanisms of AF variants identified through genetic studies.
                Methods: We summarized AF susceptibility SNPs identified by GWAS and candidate gene based association studies, and give a comprehensive functional annotation of all these AF susceptibility loci. by genomic annotation, microRNA binding prediction, promoter activity analysis, enhancer activity analysis, transcription factors binding activity prediction, expression quantitative trait loci (eQTL) analysis, long-range transcriptional regulatory function analysis, gene ontology and pathway enrichment analysis.
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The association of healthy behaviors with cognitive health expectancy in Chinese older adults: a population-based cohort study

Chengbei Hou, Yinan Lin, Zachary Zimmer, Xianghua Fang,

https://doi.org/10.18632/aging.103617 pp 16999—17021

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Hou C, Lin Y, Zimmer Z, Fang X, . The association of healthy behaviors with cognitive health expectancy in Chinese older adults: a population-based cohort study. . 12:16999-17021. https://doi.org/10.18632/aging.103617

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                TY  - JOUR
                AU  - Hou, Chengbei 
                AU  - Lin, Yinan 
                AU  - Zimmer, Zachary 
                AU  - Fang, Xianghua 
                TI  - The association of healthy behaviors with cognitive health expectancy in Chinese older adults: a population-based cohort study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103617
                DO  - 10.18632/aging.103617
                SP  - 16999
                EP  - 17021
                PY  - 
                AB  - Objective: To examine how lifestyles and leisure activities are associated with cognitive health expectancy among older adults.
                Results: For young-old (aged 65), an absolute increase in life years without cognitive impairment was found among those with a healthy diet, engaging in mental activities and in social activities. For old-old (aged 85), an absolute increase was found for men engaging in physical activities besides those. Compared with counterparts in a high risk group, the young-old in a medium-low risk group had a smaller proportion of years without cognitive impairment. Old-old in a low risk group had a greater proportion.
                Conclusion: Extra years of life gained by a healthy dietary pattern, mental activities, and social activities are free of cognitive impairment for both sexes across ages. The beneficial impact of individual and combined modifiable factors on cognitive health is most prominent in old-old.
                Methods: Data come from The Chinese Longitudinal Healthy Longevity Survey, a population-based cohort study of 27,193 participants aged 65+ conducted between 2002 and 2014. Smoking status, alcohol consumption, dietary pattern, marital status, physical, mental, social, and productive activities were assessed at baseline. Cognitive status was measured using the Chinese version of the MMSE.
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Retrospective study of gene signatures and prognostic value of m6A regulatory factor in non-small cell lung cancer using TCGA database and the verification of FTO

Hongjie Shi, Jinping Zhao, Linzhi Han, Ming Xu, Kaijie Wang, Jiajun Shi, Zhe Dong,

https://doi.org/10.18632/aging.103622 pp 17022—17037

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Shi H, Zhao J, Han L, Xu M, Wang K, Shi J, Dong Z, . Retrospective study of gene signatures and prognostic value of m6A regulatory factor in non-small cell lung cancer using TCGA database and the verification of FTO. . 12:17022-17037. https://doi.org/10.18632/aging.103622

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                TY  - JOUR
                AU  - Shi, Hongjie 
                AU  - Zhao, Jinping 
                AU  - Han, Linzhi 
                AU  - Xu, Ming 
                AU  - Wang, Kaijie 
                AU  - Shi, Jiajun 
                AU  - Dong, Zhe 
                TI  - Retrospective study of gene signatures and prognostic value of m6A regulatory factor in non-small cell lung cancer using TCGA database and the verification of FTO
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103622
                DO  - 10.18632/aging.103622
                SP  - 17022
                EP  - 17037
                PY  - 
                AB  - N6-methyladenosine (m6A) is the most common internal modification in eukaryotic mRNA. However, little is known about its role in non-small cell lung cancer (NSCLC). In this study, a total of 1017 NSCLC patients from the cancer genome atlas (TCGA) database with copy number variation (CNV) data were included. Log-rank tests and Cox regression model were used for survival analysis. The relationship between m6A regulators and clinicopathological features was evaluated using the chi-square test. The alteration of m6A regulators were related to T stage. Patients with any CNVs of regulators genes had worse overall survival (OS) than those with diploid genes. The deletion of m6A writer genes was an independent risk factor for poor OS, and the effect synergized with that of copy number gain of eraser genes. High expression of Fat mass-and obesity-associated gene (FTO) was associated with KRAS signaling up. Knockdown of FTO increased m6A content and inhibit proliferation of A549 lung cancer cell. Thus, we identified the genetic changes of m6A regulatory factors in NSCLC for the first time and found a significant relationship between these changes and poor clinical characteristics. FTO might play an important role in promoting NSCLC by decreasing m6A level and activating KRAS signaling.
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A novel hypoxic tumor microenvironment signature for predicting the survival, progression, immune responsiveness and chemoresistance of glioblastoma: a multi-omic study

Zihao Wang, Lu Gao, Xiaopeng Guo, Yaning Wang, Yu Wang, Wenbin Ma, Yi Guo, Bing Xing,

https://doi.org/10.18632/aging.103626 pp 17038—17061

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Wang Z, Gao L, Guo X, Wang Y, Wang Y, Ma W, Guo Y, Xing B, . A novel hypoxic tumor microenvironment signature for predicting the survival, progression, immune responsiveness and chemoresistance of glioblastoma: a multi-omic study. . 12:17038-17061. https://doi.org/10.18632/aging.103626

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                TY  - JOUR
                AU  - Wang, Zihao 
                AU  - Gao, Lu 
                AU  - Guo, Xiaopeng 
                AU  - Wang, Yaning 
                AU  - Wang, Yu 
                AU  - Ma, Wenbin 
                AU  - Guo, Yi 
                AU  - Xing, Bing 
                TI  - A novel hypoxic tumor microenvironment signature for predicting the survival, progression, immune responsiveness and chemoresistance of glioblastoma: a multi-omic study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103626
                DO  - 10.18632/aging.103626
                SP  - 17038
                EP  - 17061
                PY  - 
                AB  - The hypoxic tumor microenvironment (TME) was reported to promote the aggressive phenotype, progression, recurrence, and chemoresistance of glioblastoma (GBM). We developed and validated a hypoxia gene signature for individualized prognostic prediction in GBM patients. In total, 259 GBM-specific hypoxia-related genes (HRGs) were obtained in hypoxic cultured GBM cells compared with normoxic cells. By applying the k-means algorithm, TCGA GBM patients were divided into two subgroups, and the patients in Cluster 1 exhibited high HRG expression patterns, older age, and poor prognosis, which was validated in the CGGA cohort. Cox regression analyses were performed to generate an HRG-based risk score model consisting of five HRGs, which could reliably discriminate the overall survival (OS) and progression-free survival (PFS) of high- and low-risk patients in both the TCGA training and CGGA validation cohorts. Then, nomograms with the hypoxia signature for OS and PFS prediction were constructed for individualized survival prediction, better treatment decision-making, and follow-up scheduling. Finally, functional enrichment, immune infiltration, immunotherapy response prediction and chemotherapy resistance analyses demonstrated the vital roles of the hypoxic TME in the development, progression, multitherpy resistance of GBM. The hypoxia gene signature could serve as a promising prognostic predictor and potential therapeutic target to combat chemoresistant GBM.
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Evidence that dysplasia related microRNAs in Barrett’s esophagus target PD-L1 expression and contribute to the development of esophageal adenocarcinoma

Juanjuan Xu, Zhongyuan Yin, Lin Yang, Feng Wu, Jinshuo Fan, Qi Huang, Yang Jin, Guanghai Yang,

https://doi.org/10.18632/aging.103634 pp 17062—17078

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Xu J, Yin Z, Yang L, Wu F, Fan J, Huang Q, Jin Y, Yang G, . Evidence that dysplasia related microRNAs in Barrett’s esophagus target PD-L1 expression and contribute to the development of esophageal adenocarcinoma. . 12:17062-17078. https://doi.org/10.18632/aging.103634

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                TY  - JOUR
                AU  - Xu, Juanjuan 
                AU  - Yin, Zhongyuan 
                AU  - Yang, Lin 
                AU  - Wu, Feng 
                AU  - Fan, Jinshuo 
                AU  - Huang, Qi 
                AU  - Jin, Yang 
                AU  - Yang, Guanghai 
                TI  - Evidence that dysplasia related microRNAs in Barrett’s esophagus target PD-L1 expression and contribute to the development of esophageal adenocarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103634
                DO  - 10.18632/aging.103634
                SP  - 17062
                EP  - 17078
                PY  - 
                AB  - Esophageal adenocarcinoma (EAC) is the cancer arising from the esophagus, which frequently develop from Barrett&#x2019;s esophagus (BE). Extracellular vesicles (EVs), particularly exosomes, are nanosized vesicles of endosomal origin released from various types of cells that have been implicated in cancers. However, the significance of circulating exosomes during the progression of BE to EAC remains unknown. Sera exosmal microRNAs were profiled from 13 EAC and 12BE patients compared to 12 healthy controls. We found a substantial dysregulation of exosomal miRNA levels in BE compared to healthy control, and identified a unique signature of 24 up regulated and 14 down regulated miRNAs. Further validation showed exosomal miR-196a, -26b, -21, and -143 expression was significantly higher in BE and continued to have higher levels in EAC compared to healthy controls; while sera exosomal miR-378, -210, -205, and -200c-3p were significantly lower expressed in BE patients compared to compared to controls. Further, miR-378, -210, -205, and -200c-3p continue to have even lower levels in EAC patients compared to BE. Interestingly, sera expression levels of exosomal miR-15a, -16, and -193a-3p were significantly down regulated in BE PD-L1(+) patients; Sera exosomal miR-15a, -15b, -16, and -193a-3p expression levels in EAC PD-L1(+) patients were significantly lower (all p &lt; 0.01) when compared to EAC PD-L1(-) patients. More importantly, the BE-EAC group had longitudinally decreased exosomal expression levels of miR-15a, -15b, -16, and -193a-3p from BE status to their EAC progression. In conclusion, distinct microRNA expression patterns were demonstrated in circulating exosomes from Barrett&#x2019;s esophagus and esophageal adenocarcinoma; Furthermore exosomal microRNAs potentially targeting PD-L1 mRNA were down regulated in PD-L1 (+) BE and EAC patients.
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High expression of UNC5B enhances tumor proliferation, increases metastasis, and worsens prognosis in breast cancer

Shijie Wu, Xinyue Guo, Jiaojiao Zhou, Xuan Zhu, Huihui Chen, Kun Zhang, Yuexin Lu, Yiding Chen,

https://doi.org/10.18632/aging.103639 pp 17079—17098

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Wu S, Guo X, Zhou J, Zhu X, Chen H, Zhang K, Lu Y, Chen Y, . High expression of UNC5B enhances tumor proliferation, increases metastasis, and worsens prognosis in breast cancer. . 12:17079-17098. https://doi.org/10.18632/aging.103639

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                TY  - JOUR
                AU  - Wu, Shijie 
                AU  - Guo, Xinyue 
                AU  - Zhou, Jiaojiao 
                AU  - Zhu, Xuan 
                AU  - Chen, Huihui 
                AU  - Zhang, Kun 
                AU  - Lu, Yuexin 
                AU  - Chen, Yiding 
                TI  - High expression of UNC5B enhances tumor proliferation, increases metastasis, and worsens prognosis in breast cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103639
                DO  - 10.18632/aging.103639
                SP  - 17079
                EP  - 17098
                PY  - 
                AB  - UNC-5 Homolog B (UNC5B) is a member of the dependence receptor family that regulates cell survival and apoptosis in a ligand-dependent manner. UNC5B plays an important role in the development of multiple cancers, including colorectal, bladder, and thyroid cancer. However, the exact expression pattern and mechanism of UNC5B in breast cancer have not been well elucidated. Here, we showed that UNC5B expression was significantly upregulated in breast cancer using bioinformatics analysis and experimental validation. High UNC5B expression was correlated with poor overall survival in breast cancer patients. UNC5B knockdown inhibited breast cancer cell proliferation and metastasis and compromised PI3K/Akt signaling activation. In summary, UNC5B is a promising diagnostic and prognostic biomarker and targeting UNC5B is a potential strategy for individualized breast cancer treatment.
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Sirt6 is required for spermatogenesis in mice

Huafang Wei, Muhammad Babar Khawar, Wenhao Tang, Lina Wang, Liying Wang, Chao Liu, Hui Jiang, Wei Li,

https://doi.org/10.18632/aging.103641 pp 17099—17113

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Wei H, Khawar MB, Tang W, Wang L, Wang L, Liu C, Jiang H, Li W, . Sirt6 is required for spermatogenesis in mice. . 12:17099-17113. https://doi.org/10.18632/aging.103641

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                TY  - JOUR
                AU  - Wei, Huafang 
                AU  - Khawar, Muhammad Babar 
                AU  - Tang, Wenhao 
                AU  - Wang, Lina 
                AU  - Wang, Liying 
                AU  - Liu, Chao 
                AU  - Jiang, Hui 
                AU  - Li, Wei 
                TI  - Sirt6 is required for spermatogenesis in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103641
                DO  - 10.18632/aging.103641
                SP  - 17099
                EP  - 17113
                PY  - 
                AB  - SIRT6, a nuclear protein, has been implicated in a number of essential cellular processes, such as the DNA damage response, metabolic homeostasis, inflammation, tumorigenesis and aging. However, the role of Sirt6 in the regulation of spermatogenesis is yet unknown. In the present study, we successfully generated Sirt6-/- mice on a C57BL6/ICR mixed background and found that some Sirt6-/- mice survived beyond eight weeks. We further revealed that spermatogenesis in Sirt6-/- mice was arrested at the elongated spermatid stage. Sirt6-/- male mice were completely infertile and had an increased number of apoptotic spermatids. To our surprise, deacetylation activities of SIRT6 on H3K9ac, H3K18ac and H3K56c were not required for spermatogenesis. Therefore, our findings establish a novel link between Sirt6 and male fertility, suggesting an essential role of Sirt6 in spermatogenesis.
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miR-345-5p regulates adipogenesis via targeting VEGF-B

Xiaofeng Liu, Yang He, Zhaolan Feng, Jianjian Sheng, Aiwu Dong, Meiying Zhang, Lingling Cao,

https://doi.org/10.18632/aging.103649 pp 17114—17121

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Liu X, He Y, Feng Z, Sheng J, Dong A, Zhang M, Cao L, . miR-345-5p regulates adipogenesis via targeting VEGF-B. . 12:17114-17121. https://doi.org/10.18632/aging.103649

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                TY  - JOUR
                AU  - Liu, Xiaofeng 
                AU  - He, Yang 
                AU  - Feng, Zhaolan 
                AU  - Sheng, Jianjian 
                AU  - Dong, Aiwu 
                AU  - Zhang, Meiying 
                AU  - Cao, Lingling 
                TI  - miR-345-5p regulates adipogenesis via targeting VEGF-B
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103649
                DO  - 10.18632/aging.103649
                SP  - 17114
                EP  - 17121
                PY  - 
                AB  - Adipocyte differentiation involves a series of highly synergistic processes, including clone amplification, proliferation arrest, and terminal differentiation. However, the mechanisms that control these different steps remain unclear. Emerging studies support that miRNAs play an important role in regulating adipogenesis. In this study, we found that the expression of miR-345-5p decreased during adipogenic differentiation, and overexpression of miR-345-5p reduced lipid accumulation in adipocytes and the expression of adipocyte related genes essential to lipogenic transcription, fatty acid synthesis and fatty acid transport. In addition, miR-345-5p directly targeted the 3&#x2019;UTR of vascular endothelial growth factor B, and miR-345-5p mimic inhibited the expression of vascular endothelial growth factor B at both mRNA and protein levels. In conclusion, our results demonstrate that miR-345-5p inhibits adipocyte differentiation via targeting vascular endothelial growth factor B.
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Long non-coding RNA SNHG12 promotes immune escape of ovarian cancer cells through their crosstalk with M2 macrophages

Min Qian, Wanwen Ling, Zhengyi Ruan,

https://doi.org/10.18632/aging.103653 pp 17122—17136

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Qian M, Ling W, Ruan Z, . Long non-coding RNA SNHG12 promotes immune escape of ovarian cancer cells through their crosstalk with M2 macrophages. . 12:17122-17136. https://doi.org/10.18632/aging.103653

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                TY  - JOUR
                AU  - Qian, Min 
                AU  - Ling, Wanwen 
                AU  - Ruan, Zhengyi 
                TI  - Long non-coding RNA SNHG12 promotes immune escape of ovarian cancer cells through their crosstalk with M2 macrophages
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103653
                DO  - 10.18632/aging.103653
                SP  - 17122
                EP  - 17136
                PY  - 
                AB  - Accumulating evidence shows that the tumor microenvironment contributes to this phenomenon and that long non-coding RNAs (lncRNAs) are also involved in this process. In this study, we identified a new lncRNA small nucleolar RNA host gene 12 (SNHG12) and investigated its role in tumor immune escape. We analyzed the expression levels of interlukin (IL)-6R and programmed death-ligand 1 (PD-L1) in 51 ovarian cancer and 20 normal specimens by immunohistochemistry. The correlation between SNHG12 and IL-6R in clinical ovarian cancer samples was identified by RT-qPCR. We then performed SNHG12 gain- and loss-function experiments in order to investigate its role in the regulation of immune escape and the crosstalk between miR-21 and IL-6. T cell proliferation was assessed by flow cytometry. In vivo pro-immune escape activity of SNHG12 was assessed by tumor-xenograft mouse model. IL-6R and PD-L1 were found to be overexpressed in clinical ovarian cancer specimens. Meanwhile, SNHG12 and IL-6R expressions were positively correlated in clinical ovarian cancer samples. SNHG12 facilitated ovarian immune escape by promoting IL-6/miR-21 crosstalk between ovarian cancer cells and M2 macrophages. Notably, SNHG12 promoted IL-6R transcription by recruiting NF-&#x3BA;B1 to the IL-6R promoter. Our study reveals that SNHG12 facilitates ovarian cancer immune escape by upregulating IL-6R.
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The protective effects of dehydrocostus lactone against TNF-α-induced degeneration of extracellular matrix (ECM) in SW1353 cells

Lin Wang, Min Yang, Chi Zhang, Fei Huang,

https://doi.org/10.18632/aging.103657 pp 17137—17149

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Wang L, Yang M, Zhang C, Huang F, . The protective effects of dehydrocostus lactone against TNF-α-induced degeneration of extracellular matrix (ECM) in SW1353 cells. . 12:17137-17149. https://doi.org/10.18632/aging.103657

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                TY  - JOUR
                AU  - Wang, Lin 
                AU  - Yang, Min 
                AU  - Zhang, Chi 
                AU  - Huang, Fei 
                TI  - The protective effects of dehydrocostus lactone against TNF-α-induced degeneration of extracellular matrix (ECM) in SW1353 cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103657
                DO  - 10.18632/aging.103657
                SP  - 17137
                EP  - 17149
                PY  - 
                AB  - Osteoarthritis is a common joint disease that disrupts the lives of millions of people worldwide. To date, a safe and reliable treatment has not yet been announced. Excessive production of pro-inflammatory cytokines such as TNF-&#x3B1; plays an important role in the pathological development of OA. Dehydrocostus lactone (DHC) is a kind of sesquiterpene isolated from medicinal plants that has been demonstrated to play a protective role in inflammation and tumor formation. However, the effects of DHC in OA hasn&#x2019;t been reported before. In the present study, we investigated the antioxidant and protective effects of DHC in human chondrocytes against insult from tumor necrosis factor-&#x3B1; (TNF-&#x3B1;). We found that DHC inhibited oxidative stress by suppressing the production of reactive oxygen species (ROS) from TNF-&#x3B1; stimulation. Furthermore, DHC decreased the expression of pro-inflammatory cytokines induced by TNF-&#x3B1;, such as interleukin-1&#x3B2; (IL-1&#x3B2;) and interleukin-6 (IL-6). Importantly, DHC prevented the degradation of type II collagen and aggrecan, which are the main components of the extracellular matrix (ECM), by inhibiting the overexpression of matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with a thrombospondin type 1 motif (ADAMTS) induced by TNF-&#x3B1;. Mechanistically, DHC ameliorated the inflammatory response and degeneration of the articular extracellular matrix (ECM) by suppressing nuclear factor-&#x3BA;B (NF-&#x3BA;B) activation. Our results reveal that DHC possesses a beneficial effect against TNF-&#x3B1;-mediated insult in human chondrocytes, implying a potential role for DHC in the treatment of osteoarthritis (OA).
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LNK deficiency decreases obesity-induced insulin resistance by regulating GLUT4 through the PI3K-Akt-AS160 pathway in adipose tissue

Xiaozhu Zhong, Chuanfeng Ke, Zhaoxi Cai, Hao Wu, Yang Ye, Xiaolin Liang, Liqun Yu, Sushi Jiang, Jun Shen, Laiyou Wang, Meiqing Xie, Guanlei Wang, Xiaomiao Zhao,

https://doi.org/10.18632/aging.103658 pp 17150—17166

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Zhong X, Ke C, Cai Z, Wu H, Ye Y, Liang X, Yu L, Jiang S, Shen J, Wang L, Xie M, Wang G, Zhao X, . LNK deficiency decreases obesity-induced insulin resistance by regulating GLUT4 through the PI3K-Akt-AS160 pathway in adipose tissue. . 12:17150-17166. https://doi.org/10.18632/aging.103658

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                TY  - JOUR
                AU  - Zhong, Xiaozhu 
                AU  - Ke, Chuanfeng 
                AU  - Cai, Zhaoxi 
                AU  - Wu, Hao 
                AU  - Ye, Yang 
                AU  - Liang, Xiaolin 
                AU  - Yu, Liqun 
                AU  - Jiang, Sushi 
                AU  - Shen, Jun 
                AU  - Wang, Laiyou 
                AU  - Xie, Meiqing 
                AU  - Wang, Guanlei 
                AU  - Zhao, Xiaomiao 
                TI  - LNK deficiency decreases obesity-induced insulin resistance by regulating GLUT4 through the PI3K-Akt-AS160 pathway in adipose tissue
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103658
                DO  - 10.18632/aging.103658
                SP  - 17150
                EP  - 17166
                PY  - 
                AB  - In recent years, LNK, an adapter protein, has been found to be associated with metabolic diseases, including hypertension and diabetes. We found that the expression of LNK in human adipose tissue was positively correlated with serum glucose and insulin in obese people. We examined the role of LNK in insulin resistance and systemic energy metabolism using LNK-deficient mice (LNK-/-). With consumption of a high-fat diet, wild type (WT) mice accumulated more intrahepatic triglyceride, higher serum triglyceride (TG), free fatty acid (FFA) and high sensitivity C-reactive protein (hsCRP) compared with LNK-/- mice. However, there was no significant difference between LNK-/- and WT mice under normal chow diet. Meanwhile, glucose transporter 4 (GLUT4) expression in adipose tissue and insulin-stimulated glucose uptake in adipocytes were increased in LNK-/- mice. LNK-/- adipose tissue showed activated reactivity for IRS1/PI3K/Akt/AS160 signaling, and administration of a PI3K inhibitor impaired glucose uptake. In conclusion, LNK plays a pivotal role in adipose glucose transport by regulating insulin-mediated IRS1/PI3K/Akt/AS160 signaling.
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SNAI1 is a prognostic biomarker and correlated with immune infiltrates in gastrointestinal cancers

Jiaying Fang, Zan Ding,

https://doi.org/10.18632/aging.103667 pp 17167—17208

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Fang J, Ding Z, . SNAI1 is a prognostic biomarker and correlated with immune infiltrates in gastrointestinal cancers. . 12:17167-17208. https://doi.org/10.18632/aging.103667

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                TY  - JOUR
                AU  - Fang, Jiaying 
                AU  - Ding, Zan 
                TI  - SNAI1 is a prognostic biomarker and correlated with immune infiltrates in gastrointestinal cancers
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103667
                DO  - 10.18632/aging.103667
                SP  - 17167
                EP  - 17208
                PY  - 
                AB  - Epithelial-mesenchymal transition (EMT)-related genes play an important role in immunosuppression. However, the correlations of EMT-related genes to prognosis and tumor-infiltrating lymphocytes in different cancers remain unclear. TCGA, GEO databases were used to analyze the expression, prognosis, and immune infiltration of EMT markers in cancer. RT-qPCR, immunohistochemistry, and western blot were used to analysis the expression and prognosis of SNAI1 in gastrointestinal cancers. High SNAI1 expression was closely related with poorer overall survival in gastrointestinal cancers in TCGA cohort. High SNAI1 expression was closely related with poorer overall survival in gastrointestinal cancers, and was validated in GEO database. Simultaneously, high expression of SNAI1 correlates with clinical relevance of gastric cancer. Moreover, SNAI1 expression was associated with tumor-infiltrating immune cells in gastrointestinal cancers. In addition, RT-qPCR, immunohistochemistry, and western blot showed SNAI1 expression was higher in gastrointestinal cancers compared to the normal tissues. Finally, high SNAI1 expression was closely related with poorer overall survival and correlates with clinical relevance of gastrointestinal cancers in an independent validation cohort. In summary, the results approaches to suggest that SNAI1 can be used as a prognostic biomarker for determining prognosis and immune infiltration in gastrointestinal cancers.
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CircRNA circ_0072995 promotes the progression of epithelial ovarian cancer by modulating miR-147a/CDK6 axis

Jin Ding, Qingwei Wang, Nan Guo, Hao Wang, He Chen, Guantai Ni, Peiling Li,

https://doi.org/10.18632/aging.103668 pp 17209—17223

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Ding J, Wang Q, Guo N, Wang H, Chen H, Ni G, Li P, . CircRNA circ_0072995 promotes the progression of epithelial ovarian cancer by modulating miR-147a/CDK6 axis. . 12:17209-17223. https://doi.org/10.18632/aging.103668

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                TY  - JOUR
                AU  - Ding, Jin 
                AU  - Wang, Qingwei 
                AU  - Guo, Nan 
                AU  - Wang, Hao 
                AU  - Chen, He 
                AU  - Ni, Guantai 
                AU  - Li, Peiling 
                TI  - CircRNA circ_0072995 promotes the progression of epithelial ovarian cancer by modulating miR-147a/CDK6 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103668
                DO  - 10.18632/aging.103668
                SP  - 17209
                EP  - 17223
                PY  - 
                AB  - Background: Increasing evidence has indicated that circular RNAs (circRNAs) play vital roles in modulating tumor progression. However, regulatory roles and underlying mechanisms of circRNA circ_0072995 in epithelial ovarian cancer (EOC) are not well characterized.
                Results: Circ_0072995 was up regulated in EOC afflicted tissues and cell lines (HO8910 and A2780), and was mainly located in the cytoplasm. The expression of circ_0072995 was associated with the pathological grade of EOC for respective patients. Functional experiments revealed that circ_0072995 promoted EOC cell proliferation, migration, induced apoptosis, as well as enhanced tumorigenesis in vivo. Mechanistic analyses indicated that circ_0072995 may have acted as a sponge of miR-147a such as to relieve repressive effects of miR-147a upon its target CDK6.
                Conclusions: Our results revealed that circ_0072995 promoted EOC progression through the circ_0072995/miR-147a/CDK6 axis and may represent a strategy for treatment of EOC afflicted patients.
                Methods: Expression of circ_0072995 was evaluated in 40 EOC tissue samples and cell lines by qRT-PCR. The location of circ_0072995 was determined via nuclear-cytoplasmic fractionation. A series of functional experiments facilitated determinations of effects of circ_0072995 on EOC progression in vitro, and in vivo. Underlying mechanisms and influence of circ_0072995 on EOC were confirmed by bioinformatic analyses, luciferase reporter assays, qRT-PCR, and Western blotting.
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Dynamic changes in vascular size and density in transgenic mice with Alzheimer’s disease

Xiaowen Xu, Tong Meng, Qingqing Wen, Mengling Tao, Peijun Wang, Kai Zhong, Yong Shen,

https://doi.org/10.18632/aging.103672 pp 17224—17234

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Xu X, Meng T, Wen Q, Tao M, Wang P, Zhong K, Shen Y, . Dynamic changes in vascular size and density in transgenic mice with Alzheimer’s disease. . 12:17224-17234. https://doi.org/10.18632/aging.103672

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                TY  - JOUR
                AU  - Xu, Xiaowen 
                AU  - Meng, Tong 
                AU  - Wen, Qingqing 
                AU  - Tao, Mengling 
                AU  - Wang, Peijun 
                AU  - Zhong, Kai 
                AU  - Shen, Yong 
                TI  - Dynamic changes in vascular size and density in transgenic mice with Alzheimer’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103672
                DO  - 10.18632/aging.103672
                SP  - 17224
                EP  - 17234
                PY  - 
                AB  - Alzheimer&apos;s disease (AD) is one of the most common neurodegenerative diseases. Here, we used vessel size imaging to investigate the specific microvascular changes and most susceptible brain regions during AD progression in an amyloid precursor protein 23 (APP23) transgenic AD mouse model. Using 9.4 Tesla magnetic resonance imaging (MRI), the values of microvascular density (Density), mean vessel diameter (mVD), and vessel size index (VSI) were compared between APP23 and wild-type (WT) mice at 3, 6, 9, 14, and 20 months of age. Our results demonstrate that in 20-month old APP23 and WT mice, the Density values were significantly decreased, while the vascular dilatation and diameter had increased. However, a transient increase in the cortex Density at 14-months was observed in APP23 mice. Additionally, our results suggest that the hippocampus is the susceptible brain region affected by the abnormal microvascular angiogenesis during the early stages of AD. Together, our findings indicate that vessel size imaging using MRI can provide novel biomarkers for the early detection of AD, and for monitoring the effects of vascular-targeted therapeutics in AD.
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Mitophagy impairment is involved in sevoflurane-induced cognitive dysfunction in aged rats

Yeru Chen, Piao Zhang, Xianyi Lin, Huan Zhang, Jiamin Miao, Youfa Zhou, Gang Chen,

https://doi.org/10.18632/aging.103673 pp 17235—17256

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Chen Y, Zhang P, Lin X, Zhang H, Miao J, Zhou Y, Chen G, . Mitophagy impairment is involved in sevoflurane-induced cognitive dysfunction in aged rats. . 12:17235-17256. https://doi.org/10.18632/aging.103673

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                TY  - JOUR
                AU  - Chen, Yeru 
                AU  - Zhang, Piao 
                AU  - Lin, Xianyi 
                AU  - Zhang, Huan 
                AU  - Miao, Jiamin 
                AU  - Zhou, Youfa 
                AU  - Chen, Gang 
                TI  - Mitophagy impairment is involved in sevoflurane-induced cognitive dysfunction in aged rats
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103673
                DO  - 10.18632/aging.103673
                SP  - 17235
                EP  - 17256
                PY  - 
                AB  - Postoperative cognitive dysfunction (POCD) is frequently observed in elderly patients following anesthesia, but its pathophysiological mechanisms have not been fully elucidated. Sevoflurane was reported to repress autophagy in aged rat neurons; however, the role of mitophagy, which is crucial for the control of mitochondrial quality and neuronal health, in sevoflurane-induced POCD in aged rats remains undetermined. Therefore, this study investigated whether mitophagy impairment is involved in sevoflurane-induced cognitive dysfunction. We found sevoflurane treatment inhibited mitochondrial respiration and mitophagic flux, changes in mitochondria morphology, impaired lysosomal acidification, and increased Tomm20 and deceased LAMP1 accumulation were observed in H4 cell and aged rat models. Rapamycin counteracted ROS induced by sevoflurane, restored mitophagy and improved mitochondrial function. Furthermore, rapamycin ameliorated the cognitive deficits observed in aged rats given sevoflurane anesthesia as determined by the Morris water maze test; this improvement was associated with an increased number of dendritic spines and pyramidal neurons. Overexpression of PARK2, but not mutant PARK2 lacking enzyme activity, in H4 cells decreased ROS and Tomm20 accumulation and reversed mitophagy dysfunction after sevoflurane treatment. These findings suggest that mitophagy dysfunction could be a mechanism underlying sevoflurane-induced POCD and that activating mitophagy may provide a new strategy to rescue cognitive deficits.
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Inactive bowel movement and stroke are associated with increased risks of mild cognitive impairment among community-living Singapore elderly

Kai-Yong Huang, Xian-Yan Tang, Li Yang, Zhi-Yong Zhang, Kaisy Xinhong Ye, Qing-Feng Shen, Xiu Wang, Xiang-Hua Zhu, Xiao-Wei Huang, Guo-Dong Lu, Lei Feng,

https://doi.org/10.18632/aging.103674 pp 17257—17270

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Huang K, Tang X, Yang L, Zhang Z, Ye KX, Shen Q, Wang X, Zhu X, Huang X, Lu G, Feng L, . Inactive bowel movement and stroke are associated with increased risks of mild cognitive impairment among community-living Singapore elderly. . 12:17257-17270. https://doi.org/10.18632/aging.103674

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                TY  - JOUR
                AU  - Huang, Kai-Yong 
                AU  - Tang, Xian-Yan 
                AU  - Yang, Li 
                AU  - Zhang, Zhi-Yong 
                AU  - Ye, Kaisy Xinhong 
                AU  - Shen, Qing-Feng 
                AU  - Wang, Xiu 
                AU  - Zhu, Xiang-Hua 
                AU  - Huang, Xiao-Wei 
                AU  - Lu, Guo-Dong 
                AU  - Feng, Lei 
                TI  - Inactive bowel movement and stroke are associated with increased risks of mild cognitive impairment among community-living Singapore elderly
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103674
                DO  - 10.18632/aging.103674
                SP  - 17257
                EP  - 17270
                PY  - 
                AB  - Mild cognitive impairment (MCI), as a preclinical phase of dementia, provides an invaluable time window for intervention. Besides several proposed modifiable risk factors, the associations of MCI with dietary habits and bowel movement are not well clarified. We thus conducted a cross-sectional study of community-living Singapore elderly and focused on the relationship of clinically diagnosed MCI with dietary habits and bowel movement frequencies. The multiple logistic regression results showed that frequent (&#x2265;4 days per week) fruit consumption (P = 0.004), active (&#x2265;4 days per week) bowel movement within 10 minutes (P = 0.027), and years of schooling were negatively associated with MCI occurrence. In contrast, medical comorbidities including hypertension, stroke, and cataract/glaucoma were found to be risk factors. Furthermore, a Bayesian network model of causal inference detected five hypothesized causal-association paths leading to MCI, namely bowel movement, stroke, years of schooling via fruit consumption, hypertension via stroke and hypertension via cataract/glaucoma. The combination of the two direct factors (inactive bowel movement and stroke) reached a maximum conditional probability of 60.00% for MCI occurrence. Taken together, this study was the first to link bowel movement with MCI occurrence. In addition, it suggested five modifiable hypothesized causal-association paths to MCI.
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Profiling of circular RNAs in age-related cataract reveals circZNF292 as an antioxidant by sponging miR-23b-3p

Shuqi Liang, Shengqian Dou, Wenfeng Li, Yusen Huang,

https://doi.org/10.18632/aging.103683 pp 17271—17287

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Liang S, Dou S, Li W, Huang Y, . Profiling of circular RNAs in age-related cataract reveals circZNF292 as an antioxidant by sponging miR-23b-3p. . 12:17271-17287. https://doi.org/10.18632/aging.103683

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                TY  - JOUR
                AU  - Liang, Shuqi 
                AU  - Dou, Shengqian 
                AU  - Li, Wenfeng 
                AU  - Huang, Yusen 
                TI  - Profiling of circular RNAs in age-related cataract reveals circZNF292 as an antioxidant by sponging miR-23b-3p
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103683
                DO  - 10.18632/aging.103683
                SP  - 17271
                EP  - 17287
                PY  - 
                AB  - Age-related cataract (ARC) is one of the major causes of visual impairment and reversible blindness worldwide. Accumulating evidence has revealed that circular RNAs (circRNAs) are involved in multiple regulatory processes in various ocular diseases. However, the expression profile, regulatory roles, and underlying mechanisms of circRNAs in ARC remain largely unknown. Herein we deep-sequenced circRNAs of anterior lens capsules from normal and ARC lenses, and detected 23,787 candidate circRNAs. Of these, 466 were significantly differentially expressed, and a higher correlation in down-regulated circRNAs between ARC and diabetic cataract was observed compared with up-regulated ones. Subsequent bioinformatics analysis disclosed that certain differentially expressed circRNAs participated in oxidative stress and apoptosis-related signaling pathways in ARC. Notably, the level of circZNF292 was significantly decreased, while miR-23b-3p was significantly increased in ARC. The target region prediction and dual-luciferase reporter assays proved that circZNF292 acted as a competitive endogenous RNA to regulate the expression of anti-oxidative genes through competing with miR-23b-3p. Our results indicate that circZNF292, a down-regulated circRNA in the anterior lens capsule of ARC patients, may be involved in resistance to oxidative damage and apoptosis of lens epithelial cells by sponging miR-23b-3p, providing a potential target for prevention and treatment of ARC.
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Male patients with TERT mutation may be more likely to benefit from immunotherapy, especially for melanoma

Jia Li, Zhaoyan Li, Chenyue Zhang, Chenxing Zhang, Haiyong Wang,

https://doi.org/10.18632/aging.103684 pp 17288—17294

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Li J, Li Z, Zhang C, Zhang C, Wang H, . Male patients with TERT mutation may be more likely to benefit from immunotherapy, especially for melanoma. . 12:17288-17294. https://doi.org/10.18632/aging.103684

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                TY  - JOUR
                AU  - Li, Jia 
                AU  - Li, Zhaoyan 
                AU  - Zhang, Chenyue 
                AU  - Zhang, Chenxing 
                AU  - Wang, Haiyong 
                TI  - Male patients with TERT mutation may be more likely to benefit from immunotherapy, especially for melanoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103684
                DO  - 10.18632/aging.103684
                SP  - 17288
                EP  - 17294
                PY  - 
                AB  - Genomic mutation may be key factors for sex-biased disparities in cancer diagnosis, prognosis and prediction of treatment response. Current study has revealed that sex-based dimorphism on the efficacy of immune checkpoint inhibitors (ICIs) in various cancers and confirmed that male patients can benefit more from immunotherapy. However, only a subset of male patients responds well to ICIs. Therefore, biomarkers are desperately needed to identify the group of patients who may be more likely to benefit from ICIs. With the availability of the cBioPortal database, we identified that TERT mutation may serve as a sex-specific cancer biomarker and TERT mutation frequency of melanoma was higher in male patients. Notably, we found that male patients with TERT mutation may be more likely to benefit from immunotherapy (p = 0.006), especially for melanoma (p &lt; 0.001). Therefore, our research provides a possible direction for the exploration of immunotherapy prediction biomarkers based on sex difference.
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Relation between left atrial structure and lacunar infarction in patients with hypertension

Ting Sun, Tong Xie, Alian Zhang, Li Fan, Zuojun Xu, Xin Chen, Zhicheng Fan, Changqian Wang,

https://doi.org/10.18632/aging.103697 pp 17295—17304

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Sun T, Xie T, Zhang A, Fan L, Xu Z, Chen X, Fan Z, Wang C, . Relation between left atrial structure and lacunar infarction in patients with hypertension. . 12:17295-17304. https://doi.org/10.18632/aging.103697

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                TY  - JOUR
                AU  - Sun, Ting 
                AU  - Xie, Tong 
                AU  - Zhang, Alian 
                AU  - Fan, Li 
                AU  - Xu, Zuojun 
                AU  - Chen, Xin 
                AU  - Fan, Zhicheng 
                AU  - Wang, Changqian 
                TI  - Relation between left atrial structure and lacunar infarction in patients with hypertension
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103697
                DO  - 10.18632/aging.103697
                SP  - 17295
                EP  - 17304
                PY  - 
                AB  - A lacunar infarction (LACI) can cause damage to the surrounding brain tissue and place an individual at greater risk for future major stroke. LACI is associated with hypertension and hypertension is associated with left atrial enlargement. It is important to identify a high-risk patient who is more vulnerable to suffering a LACI in hypertensive group. So, we studied whether left atrium size is an independent risk predictor for LACI in hypertensive patients. We performed cross-sectional analysis of 365 patients with hypertension at Shanghai Ninth People&#x2019;s Hospital from January 2016 to January 2017. The results showed that left atrial diameter(LAD), left atrial volume (LAV) and the ratio of left atrial diameter to left ventricular diameter (LAD/LVD) were significantly associated with LACI in hypertensive patients. Based on the ROC curve analysis, the area under the ROC curve (AUC) of LAV used to predict LACI was 0.737 (95% CI: 0.686 &#x2013; 0.788), and the AUC of LAD/LVD was 0.784 (95% CI: 0.737 &#x2013; 0.830). The optimal cut-off value for LAV was 30.14, and the sensitivity and specificity were 72% and 63%, respectively. The optimal cut-off value for LAD/LVD was 0.757, and the sensitivity and specificity were 77% and 70%, respectively. LAV or LAD/LVD played an important role in LACI with hypertension and could be an independent risk factor in hypertensive patients.
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Chloride intracellular channel protein 2: prognostic marker and correlation with PD-1/PD-L1 in breast cancer

Tao Xu, Zhi Wang, Menglu Dong, Di Wu, Shujie Liao, Xingrui Li,

https://doi.org/10.18632/aging.103712 pp 17305—17327

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Xu T, Wang Z, Dong M, Wu D, Liao S, Li X, . Chloride intracellular channel protein 2: prognostic marker and correlation with PD-1/PD-L1 in breast cancer. . 12:17305-17327. https://doi.org/10.18632/aging.103712

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                TY  - JOUR
                AU  - Xu, Tao 
                AU  - Wang, Zhi 
                AU  - Dong, Menglu 
                AU  - Wu, Di 
                AU  - Liao, Shujie 
                AU  - Li, Xingrui 
                TI  - Chloride intracellular channel protein 2: prognostic marker and correlation with PD-1/PD-L1 in breast cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103712
                DO  - 10.18632/aging.103712
                SP  - 17305
                EP  - 17327
                PY  - 
                AB  - Immune checkpoint inhibition has emerged as an effective treatment for multiple solid tumors, including advanced-stage breast cancer (BC). During the past decade, the US Food and Drug Administration has approved a number of agents for immune checkpoint blockade (ICB). However, the limited data on monotherapy anti-tumor activity in BC underscores the need for robust predictive biomarker development. Here, we used weighted gene coexpression network analysis of genes differentially expressed between BC and normal tissue to identify genes coexpressed with programmed death-1 (PD-1) and its ligand (PD-L1). Tumor Immune Estimation Resource and Gene Expression Profiling Interaction Analysis were used to assess the relationship between gene expression and the abundance of tumor-infiltrating lymphocytes (TILs). We found that chloride intracellular channel protein 2 (CLIC2) was not only coexpressed with PD-1 and PD-L1, but its increased expression was associated with a favorable prognosis and enrichment of multiple TIL types, particularly CD8+ T cells. These results suggest that CLIC2 is a potentially useful biomarker for identifying BC patients who could benefit from ICB.
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Functional connectivity network estimation with an inter-similarity prior for mild cognitive impairment classification

Weikai Li, Xiaowen Xu, Wei Jiang, Peijun Wang, Xin Gao,

https://doi.org/10.18632/aging.103719 pp 17328—17342

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Li W, Xu X, Jiang W, Wang P, Gao X, . Functional connectivity network estimation with an inter-similarity prior for mild cognitive impairment classification. . 12:17328-17342. https://doi.org/10.18632/aging.103719

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                TY  - JOUR
                AU  - Li, Weikai 
                AU  - Xu, Xiaowen 
                AU  - Jiang, Wei 
                AU  - Wang, Peijun 
                AU  - Gao, Xin 
                TI  - Functional connectivity network estimation with an inter-similarity prior for mild cognitive impairment classification
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103719
                DO  - 10.18632/aging.103719
                SP  - 17328
                EP  - 17342
                PY  - 
                AB  - Functional connectivity network (FCN) analysis is an effective technique for modeling human brain patterns and diagnosing neurological disorders such as Alzheimer&#x2019;s disease (AD) and its early stage, Mild Cognitive Impairment. However, accurately estimating biologically meaningful and discriminative FCNs remains challenging due to the poor quality of functional magnetic resonance imaging (fMRI) data and our limited understanding of the human brain. Inspired by the inter-similarity nature of FCNs, similar regions of interest tend to share similar connection patterns. Here, we propose a functional brain network modeling scheme by encoding Inter-similarity prior into a graph-regularization term, which can be easily solved with an efficient optimization algorithm. To illustrate its effectiveness, we conducted experiments to distinguish Mild Cognitive Impairment from normal controls based on their respective FCNs. Our method outperformed the baseline and state-of-the-art methods by achieving an 88.19% classification accuracy. Furthermore, post hoc inspection of the informative features showed that our method yielded more biologically meaningful functional brain connectivity.
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High hsa_circ_0020123 expression indicates poor progression to non-small cell lung cancer by regulating the miR-495/HOXC9 axis

Rui Bi, Wei Wei, Yunhui Lu, Fengqing Hu, Xuhui Yang, Yuan Zhong, Lifei Meng, Mingsong Wang, Lianyong Jiang, Xiao Xie,

https://doi.org/10.18632/aging.103722 pp 17343—17352

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Bi R, Wei W, Lu Y, Hu F, Yang X, Zhong Y, Meng L, Wang M, Jiang L, Xie X, . High hsa_circ_0020123 expression indicates poor progression to non-small cell lung cancer by regulating the miR-495/HOXC9 axis. . 12:17343-17352. https://doi.org/10.18632/aging.103722

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                TY  - JOUR
                AU  - Bi, Rui 
                AU  - Wei, Wei 
                AU  - Lu, Yunhui 
                AU  - Hu, Fengqing 
                AU  - Yang, Xuhui 
                AU  - Zhong, Yuan 
                AU  - Meng, Lifei 
                AU  - Wang, Mingsong 
                AU  - Jiang, Lianyong 
                AU  - Xie, Xiao 
                TI  - High hsa_circ_0020123 expression indicates poor progression to non-small cell lung cancer by regulating the miR-495/HOXC9 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103722
                DO  - 10.18632/aging.103722
                SP  - 17343
                EP  - 17352
                PY  - 
                AB  - Circular RNAs (circRNAs) belong to non-protein-coding RNAs that regulate different pathophysiological procedures. Upregulation of hsa_circ_0020123 is found in non-small cell lung cancer (NSCLC); however, its activity and functions are not clear. In this study, the results showed that hsa_circ_0020123 expression increased in both tumor tissues and NSCLC cells. A higher hsa_circ_0020123 expression also led to poor prognoses among NSCLC patients assayed via FISH. The data of FISH also confirmed that hsa_circ_0020123 primarily had a cytoplasmic location. Hsa_circ_0020123 knockdown caused a significant decrease in nude mouse xenograft growth. Bioinformatics analyses and dual luciferase reporter assays confirmed that hsa_circ_0020123 was an miR-495 sponge and that the HOXC9 gene was a miR-495 target. The miR-495 downregulation reversed cell migration and proliferation inhibition induced by hsa_circ_0020123 silencing in vitro. HOXC9 overexpression reversed miR-495-induced inhibition of cell migration and proliferation. The dual luciferase reporter assay demonstrated that hsa_circ_0020123 interacted with miR-495 by binding to the HOXC9 3&#x2032;-UTR to suppresses post-transcriptional HOXC9 expression. Taken together, our study found that hsa_circ_0020123 functioned like a tumor promoter via a novel hsa_circ_0020123/miR-495/HOXC9 axis, highlighting its possibility as a new NSCLC therapeutic target.
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Taurine suppresses ROS-dependent autophagy via activating Akt/mTOR signaling pathway in calcium oxalate crystals-induced renal tubular epithelial cell injury

Yan Sun, Shiting Dai, Jin Tao, Yunlong Li, Ziqi He, Quan Liu, Jiawen Zhao, Yaoliang Deng, Juening Kang, Xuepei Zhang, Sixing Yang, Yunlong Liu,

https://doi.org/10.18632/aging.103730 pp 17353—17366

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Sun Y, Dai S, Tao J, Li Y, He Z, Liu Q, Zhao J, Deng Y, Kang J, Zhang X, Yang S, Liu Y, . Taurine suppresses ROS-dependent autophagy via activating Akt/mTOR signaling pathway in calcium oxalate crystals-induced renal tubular epithelial cell injury. . 12:17353-17366. https://doi.org/10.18632/aging.103730

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                TY  - JOUR
                AU  - Sun, Yan 
                AU  - Dai, Shiting 
                AU  - Tao, Jin 
                AU  - Li, Yunlong 
                AU  - He, Ziqi 
                AU  - Liu, Quan 
                AU  - Zhao, Jiawen 
                AU  - Deng, Yaoliang 
                AU  - Kang, Juening 
                AU  - Zhang, Xuepei 
                AU  - Yang, Sixing 
                AU  - Liu, Yunlong 
                TI  - Taurine suppresses ROS-dependent autophagy via activating Akt/mTOR signaling pathway in calcium oxalate crystals-induced renal tubular epithelial cell injury
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103730
                DO  - 10.18632/aging.103730
                SP  - 17353
                EP  - 17366
                PY  - 
                AB  - Oxidative stress and autophagy are the key promoters of calcium oxalate (CaOx) nephrolithiasis. Taurine is an antioxidant that plays a protective role in the pathogenesis of kidney disease. Previous studies found that taurine suppressed cellular oxidative stress, and inhibited autophagy activation. However, the effect of taurine on CaOx kidney stone formation remains unknown. In the present work, we explored the regulatory effects of taurine on CaOx crystals-induced HK-2 cell injury. Results showed that pretreatment with taurine significantly enhanced the viability of HK-2 cells and ameliorated kidney tissue injury induced by CaOx crystals. Taurine also markedly reduced the levels of inflammatory cytokines, apoptosis, and CaOx crystals deposition. Furthermore, we observed that taurine supplementation alleviated CaOx crystals-induced autophagy. Mechanism studies showed that taurine reduced oxidative stress via increasing SOD activity, reducing MDA concentration, alleviating mitochondrial oxidative injury, and decreasing the production of intracellular ROS. Taurine treatment also effectively activated Akt/mTOR signaling pathway in CaOx crystals-induced HK-2 cells both in vitro and in vivo. In summary, the current study shows that taurine inhibits ROS-dependent autophagy via activating Akt/mTOR signaling pathway in CaOx crystals-induced HK-2 cell and kidney injury, suggesting that taurine may serve as an effective therapeutic agent for the treatment of CaOx nephrolithiasis.
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G-protein coupled estrogen receptor activation protects the viability of hyperoxia-treated primary murine retinal microglia by reducing ER stress

Rong Li, Yao Wang, Pei Chen, Jiamin Meng, Hongbing Zhang,

https://doi.org/10.18632/aging.103733 pp 17367—17379

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Li R, Wang Y, Chen P, Meng J, Zhang H, . G-protein coupled estrogen receptor activation protects the viability of hyperoxia-treated primary murine retinal microglia by reducing ER stress. . 12:17367-17379. https://doi.org/10.18632/aging.103733

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                TY  - JOUR
                AU  - Li, Rong 
                AU  - Wang, Yao 
                AU  - Chen, Pei 
                AU  - Meng, Jiamin 
                AU  - Zhang, Hongbing 
                TI  - G-protein coupled estrogen receptor activation protects the viability of hyperoxia-treated primary murine retinal microglia by reducing ER stress
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103733
                DO  - 10.18632/aging.103733
                SP  - 17367
                EP  - 17379
                PY  - 
                AB  - In this study, we investigated the effects of G-protein coupled estrogen receptor (GPER) activation in the early phase of retinopathy of prematurity (ROP) and its association with endoplasmic reticulum (ER) stress using primary murine retinal microglia as an experimental model. Fluorescence microscopy results show that the CD11c-positive primary retinal microglia in vitro cultured for 14 days were GPER-positive. GPER activation using GPER-agonist G-1 reduced autophagy and increased the viability of the hyperoxia-treated primary murine retinal microglia. Furthermore, GPER activation reduced the expression of ER stress-related proteins, IRE1&#x3B1;, PERK and ATF6 in the hyperoxia-treated primary murine retinal microglia compared to the corresponding controls. GPER activation significantly reduced a time-dependent increase in IP3R-dependent calcium release from the ER, thereby maintaining higher calcium levels in the ER of hyperoxia-treated primary retinal microglia. However, the protective effects of G-1 on the hyperoxia-treated primary retinal microglia were eliminated by inactivation of GPER using the GPER-antagonist, G-15. In conclusion, our study demonstrates that GPER activation enhances the survival of hyperoxia-treated primary retinal microglia by reducing ER stress. Our study demonstrates the therapeutic potential of GPER agonists such as G-1 in the early phase of ROP.
                ER  -

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Identification of a cullin5-RING E3 ligase transcriptome signature in glioblastoma multiforme

Shuhua Zheng, Zhenhao Li,

https://doi.org/10.18632/aging.103737 pp 17380—17392

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Zheng S, Li Z, . Identification of a cullin5-RING E3 ligase transcriptome signature in glioblastoma multiforme. . 12:17380-17392. https://doi.org/10.18632/aging.103737

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                TY  - JOUR
                AU  - Zheng, Shuhua 
                AU  - Li, Zhenhao 
                TI  - Identification of a cullin5-RING E3 ligase transcriptome signature in glioblastoma multiforme
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103737
                DO  - 10.18632/aging.103737
                SP  - 17380
                EP  - 17392
                PY  - 
                AB  - Glioblastoma multiforme (GBM) is the deadliest type of brain tumor. The median survival time for patients with GBM is only 15 months, even following maximal surgical resection and chemotherapy and radiation therapy. A genetic biomarker could enable a paradigm shift in precise diagnosis, personalized therapeutics and prognosis. In this study, we employed the Chinese Glioma Genome Atlas, The Cancer Genome Atlas, and the Ivy Glioblastoma Atlas Project databases for RNA sequencing (RNA-seq) analysis and clinicopathological studies. We demonstrated that elevated expression of the RNF7, TCEB1, SOCS1 and SOCS3 genes, which encode components of cullin5-RING E3 ligase (CRL5), predict unfavorable GBM prognoses. In GBM and glioma cases carrying IDH1 mutations, SOCS1 and SOCS3 methylation was increased and their expression was downregulated. This study has thus identified a simple transcriptome signature for GBM prognosis.
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Physical performance and chronic kidney disease development in elderly adults: results from a nationwide cohort study

Young Su Joo, Jong Hyun Jhee, Hyung-Woo Kim, Seung Hyeok Han, Tae-Hyun Yoo, Shin-Wook Kang, Jung Tak Park,

https://doi.org/10.18632/aging.103741 pp 17393—17417

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Joo YS, Jhee JH, Kim H, Han SH, Yoo T, Kang S, Park JT, . Physical performance and chronic kidney disease development in elderly adults: results from a nationwide cohort study. . 12:17393-17417. https://doi.org/10.18632/aging.103741

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                TY  - JOUR
                AU  - Joo, Young Su 
                AU  - Jhee, Jong Hyun 
                AU  - Kim, Hyung-Woo 
                AU  - Han, Seung Hyeok 
                AU  - Yoo, Tae-Hyun 
                AU  - Kang, Shin-Wook 
                AU  - Park, Jung Tak 
                TI  - Physical performance and chronic kidney disease development in elderly adults: results from a nationwide cohort study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103741
                DO  - 10.18632/aging.103741
                SP  - 17393
                EP  - 17417
                PY  - 
                AB  - Sarcopenia, which is characterized by muscle mass and physical performance, is closely associated with morbidities and mortality, especially among the elderly. However, the effect of physical performance on chronic kidney disease (CKD) development is not yet fully elucidated. A total of 30,871 adults aged 66 years with preserved renal function who underwent health screening examinations were evaluated. Physical performance was assessed using a 3-m timed up and go (TUG) test and the one-leg stand (OLS) test. The primary outcome was the development of CKD, defined as at least two consecutive measurements of estimated glomerular filtration rate &lt; 60 mL/min/1.73 m2. The rates of mortality and incident CKD development were significantly elevated with increases in TUG test scores but not in OLS scores. In the Cox hazards model, the highest TUG test score tertile was associated with an increased risk for CKD development (hazard ratio, 1.23; 95% confidence interval, 1.10-1.38) compared with the lowest tertile. No significant relationship was observed between OLS score and incident CKD risk. Poor physical performance, assessed using the TUG test, was related to an increased risk of CKD development.
                ER  -

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Identification of subtype-specific genes signature by WGCNA for prognostic prediction in diffuse type gastric cancer

Qi Zhou, Li-Qiang Zhou, Shi-Hao Li, Yi-Wu Yuan, Li Liu, Jin-Liang Wang, Deng-Zhong Wu, You Wu, Lin Xin,

https://doi.org/10.18632/aging.103743 pp 17418—17435

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Zhou Q, Zhou L, Li S, Yuan Y, Liu L, Wang J, Wu D, Wu Y, Xin L, . Identification of subtype-specific genes signature by WGCNA for prognostic prediction in diffuse type gastric cancer. . 12:17418-17435. https://doi.org/10.18632/aging.103743

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                TY  - JOUR
                AU  - Zhou, Qi 
                AU  - Zhou, Li-Qiang 
                AU  - Li, Shi-Hao 
                AU  - Yuan, Yi-Wu 
                AU  - Liu, Li 
                AU  - Wang, Jin-Liang 
                AU  - Wu, Deng-Zhong 
                AU  - Wu, You 
                AU  - Xin, Lin 
                TI  - Identification of subtype-specific genes signature by WGCNA for prognostic prediction in diffuse type gastric cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103743
                DO  - 10.18632/aging.103743
                SP  - 17418
                EP  - 17435
                PY  - 
                AB  - Background: Gastric cancer is a common malignancy and had poor response to treatment due to its strong heterogeneity. This study aimed to identify essential genes associated with diffuse type gastric cancer and construct a powerful prognostic model.
                Results: We conducted a weighted gene co-expression network analysis (WGCN) using transcripts per million (TPM) expression data from The Cancer Genome Atlas (TCGA) to find out the module related with diffuse type gastric cancer. Combining Least Absolute Shrinkage and Selection Operator (LASSO) with multi-cox regression, the 10 specific genes risk score model of diffuse type gastric cancer was established. The concordance index (0.97), the area under the respective ROC curves (AUCs) (1-years: 0.98; 3-years: 1; 5-years: 1) and survival difference of high- and low risk groups (p=2.84e-10) of this model in TCGA dataset were obtained. The moderate predicting performance was observed in the independent cohort of GSE15459 and GSE62254. The results of the gene set enrichment analysis (GSEA) using high-and low risk group as phenotype indicated differential expression of tumor-related pathways.
                Conclusion: Thus, we constructed a reliable prognostic model for diffuse type gastric cancer, which should be beneficial for clinical therapeutic decision-making.
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Jinmaitong ameliorates diabetic peripheral neuropathy in streptozotocin-induced diabetic rats by modulating gut microbiota and neuregulin 1

Jun Xie, Wei Song, Xiaochun Liang, Qian Zhang, Yue Shi, Wei Liu, Xiaohu Shi,

https://doi.org/10.18632/aging.103750 pp 17436—17458

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Xie J, Song W, Liang X, Zhang Q, Shi Y, Liu W, Shi X, . Jinmaitong ameliorates diabetic peripheral neuropathy in streptozotocin-induced diabetic rats by modulating gut microbiota and neuregulin 1. . 12:17436-17458. https://doi.org/10.18632/aging.103750

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                TY  - JOUR
                AU  - Xie, Jun 
                AU  - Song, Wei 
                AU  - Liang, Xiaochun 
                AU  - Zhang, Qian 
                AU  - Shi, Yue 
                AU  - Liu, Wei 
                AU  - Shi, Xiaohu 
                TI  - Jinmaitong ameliorates diabetic peripheral neuropathy in streptozotocin-induced diabetic rats by modulating gut microbiota and neuregulin 1
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103750
                DO  - 10.18632/aging.103750
                SP  - 17436
                EP  - 17458
                PY  - 
                AB  - Jinmaitong (JMT), a compound prescription of traditional Chinese medicine, has long been used as a therapy for diabetic peripheral neuropathy (DPN). However, the neuroprotective mechanisms of JMT and its effect on gut microbiota remained unknown. Here, we examined the effects of JMT on behavior, pathomorphology and gut microbiota in streptozotocin (STZ)-induced DPN rats. Compared to distilled water administration, JMT reversed decreases in mechanical withdraw threshold and intraepidermal nerve fiber density, improved neurological morphology of sciatic nerves, increased serum neuregulin 1 (NRG1) level and contactin-associated protein (Caspr)-positive paranodes, and decreased amyloid precursor protein (APP) accumulation in DPN rats. More importantly, JMT enriched nine species of the gut microbiota of DPN rats, helping to prevent dysbiosis. Among these species, p_Actinobacteria, p_Proteobacteria and c_Actinobacteria were negatively correlated with DPN phenotypes and positively correlated with serum NRG1 level. These results indicate that JMT may exert a neuroprotective effect by modulating phenotype-associated gut microbiota and increasing serum NRG1 level in STZ-induced DPN rats. JMT may therefore be an effective complementary and alternative anti-DPN therapy.
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LINC00160 mediates sunitinib resistance in renal cell carcinoma via SAA1 that is implicated in STAT3 activation and compound transportation

Gong Cheng, Yuenan Liu, Lilong Liu, Hailong Ruan, Qi Cao, Zhengshuai Song, Lin Bao, Tianbo Xu, Zhiyong Xiong, Jingchong Liu, Di Liu, Huageng Liang, Guosong Jiang, Xiong Yang, Hongmei Yang, Ke Chen, Xiaoping Zhang,

https://doi.org/10.18632/aging.103755 pp 17459—17479

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Cheng G, Liu Y, Liu L, Ruan H, Cao Q, Song Z, Bao L, Xu T, Xiong Z, Liu J, Liu D, Liang H, Jiang G, et al, . LINC00160 mediates sunitinib resistance in renal cell carcinoma via SAA1 that is implicated in STAT3 activation and compound transportation. . 12:17459-17479. https://doi.org/10.18632/aging.103755

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                TY  - JOUR
                AU  - Cheng, Gong 
                AU  - Liu, Yuenan 
                AU  - Liu, Lilong 
                AU  - Ruan, Hailong 
                AU  - Cao, Qi 
                AU  - Song, Zhengshuai 
                AU  - Bao, Lin 
                AU  - Xu, Tianbo 
                AU  - Xiong, Zhiyong 
                AU  - Liu, Jingchong 
                AU  - Liu, Di 
                AU  - Liang, Huageng 
                AU  - Jiang, Guosong 
                AU  - Yang, Xiong 
                AU  - Yang, Hongmei 
                AU  - Chen, Ke 
                AU  - Zhang, Xiaoping 
                TI  - LINC00160 mediates sunitinib resistance in renal cell carcinoma via SAA1 that is implicated in STAT3 activation and compound transportation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103755
                DO  - 10.18632/aging.103755
                SP  - 17459
                EP  - 17479
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Cheng, Gong 
                AU  - Liu, Yuenan 
                AU  - Liu, Lilong 
                AU  - Ruan, Hailong 
                AU  - Cao, Qi 
                AU  - Song, Zhengshuai 
                AU  - Bao, Lin 
                AU  - Xu, Tianbo 
                AU  - Xiong, Zhiyong 
                AU  - Liu, Jingchong 
                AU  - Liu, Di 
                AU  - Liang, Huageng 
                AU  - Jiang, Guosong 
                AU  - Yang, Xiong 
                AU  - Yang, Hongmei 
                AU  - Chen, Ke 
                AU  - Zhang, Xiaoping 
                TI  - LINC00160 mediates sunitinib resistance in renal cell carcinoma via SAA1 that is implicated in STAT3 activation and compound transportation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103755
                DO  - 10.18632/aging.103755
                SP  - 17459
                EP  - 17479
                PY  - 
                AB  - Patients with advanced renal cell carcinoma who are resistant to sunitinib currently have limited clinical options for treatment. Therefore, it is necessary to explore the biological basis of sunitinib resistance and to uncover new targets for the intervention of sunitinib resistance. In this study, we identified that LINC00160 was associated with sunitinib resistance in renal cell carcinoma. Resistant tumor cells highly expressed LINC00160 to recruit transcriptional factor TFAP2A, which bound to SAA1 promoter regions and activated its expression. On one hand, SAA1 linked to ABCB1 protein, which facilitated sunitinib cellular efflux and diminished drug accumulation. On the other hand, SAA1 stimulated JAK-STAT signaling pathways, which countered cellular survival inhibition from drug. All these regulatory networks were well organized and collaborated, thus promoting sunitinib resistance in renal cell carcinoma. LINC00160 mediates sunitinib resistance in renal cell carcinoma via SAA1 that is implicated in STAT3 activation and compound transportation, which offers an opportunity for targeted intervention and molecular therapies in the future.
                ER  -

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Fecal microbiota transplantation alters the susceptibility of obese rats to type 2 diabetes mellitus

Lijing Zhang, Wen Zhou, Libin Zhan, Shenglin Hou, Chunyan Zhao, Tingting Bi, Xiaoguang Lu,

https://doi.org/10.18632/aging.103756 pp 17480—17502

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Zhang L, Zhou W, Zhan L, Hou S, Zhao C, Bi T, Lu X, . Fecal microbiota transplantation alters the susceptibility of obese rats to type 2 diabetes mellitus. . 12:17480-17502. https://doi.org/10.18632/aging.103756

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                TY  - JOUR
                AU  - Zhang, Lijing 
                AU  - Zhou, Wen 
                AU  - Zhan, Libin 
                AU  - Hou, Shenglin 
                AU  - Zhao, Chunyan 
                AU  - Bi, Tingting 
                AU  - Lu, Xiaoguang 
                TI  - Fecal microbiota transplantation alters the susceptibility of obese rats to type 2 diabetes mellitus
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103756
                DO  - 10.18632/aging.103756
                SP  - 17480
                EP  - 17502
                PY  - 
                AB  - Obesity is one of the susceptibility factors for type 2 diabetes (T2DM), both of which could accelerate the aging of the body and bring many hazards. A causal relationship is present between intestinal microbiota and body metabolism, but how the microbiota play a role in the progression of obesity to T2DM has not been elucidated. In this study, we transplanted healthy or obese-T2DM intestinal microbiota to ZDF and LZ rats, and used 16S rRNA and targeted metabonomics to evaluate the directional effect of the microbiota on the susceptibility of obese rats to T2DM. The glycolipid metabolism phenotype could be changed bidirectionally in obese rats instead of in lean ones. One possible mechanism is that the microbiota and metabolites alter the structure of the intestinal tract, and improve insulin and leptin resistance through JAK2 / IRS / Akt pathway. It is worth noting that 7 genera, such as Lactobacillus, Clostridium and Roche, can regulate 15 metabolites, such as 3-indolpropionic acid, acetic acid and docosahexaenoic acid, and have a significant improvement on glycolipid metabolism phenotype. Attention to intestinal homeostasis may be the key to controlling obesity and preventing T2DM.
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Transcriptome analysis of duck embryo fibroblasts for the dynamic response to duck tembusu virus infection and dual regulation of apoptosis genes

Yuhong Pan, Anchun Cheng, Xingcui Zhang, Mingshu Wang, Shun Chen, Dekang Zhu, Mafeng Liu, Xinxin Zhao, Qiao Yang, Ying Wu, Juan Huang, Shaqiu Zhang, Sai Mao, Xumin Ou, Qun Gao, Yanling Yu, Yunya Liu, Ling Zhang, Zhongqiong Yin, Bo Jing, Bin Tian, Leichang Pan, Mujeeb Ur Rehman, Xiaoyue Chen, Renyong Jia,

https://doi.org/10.18632/aging.103759 pp 17503—17527

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Pan Y, Cheng A, Zhang X, Wang M, Chen S, Zhu D, Liu M, Zhao X, Yang Q, Wu Y, Huang J, Zhang S, Mao S, et al, . Transcriptome analysis of duck embryo fibroblasts for the dynamic response to duck tembusu virus infection and dual regulation of apoptosis genes. . 12:17503-17527. https://doi.org/10.18632/aging.103759

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                TY  - JOUR
                AU  - Pan, Yuhong 
                AU  - Cheng, Anchun 
                AU  - Zhang, Xingcui 
                AU  - Wang, Mingshu 
                AU  - Chen, Shun 
                AU  - Zhu, Dekang 
                AU  - Liu, Mafeng 
                AU  - Zhao, Xinxin 
                AU  - Yang, Qiao 
                AU  - Wu, Ying 
                AU  - Huang, Juan 
                AU  - Zhang, Shaqiu 
                AU  - Mao, Sai 
                AU  - Ou, Xumin 
                AU  - Gao, Qun 
                AU  - Yu, Yanling 
                AU  - Liu, Yunya 
                AU  - Zhang, Ling 
                AU  - Yin, Zhongqiong 
                AU  - Jing, Bo 
                AU  - Tian, Bin 
                AU  - Pan, Leichang 
                AU  - Rehman, Mujeeb Ur 
                AU  - Chen, Xiaoyue 
                AU  - Jia, Renyong 
                TI  - Transcriptome analysis of duck embryo fibroblasts for the dynamic response to duck tembusu virus infection and dual regulation of apoptosis genes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103759
                DO  - 10.18632/aging.103759
                SP  - 17503
                EP  - 17527
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Pan, Yuhong 
                AU  - Cheng, Anchun 
                AU  - Zhang, Xingcui 
                AU  - Wang, Mingshu 
                AU  - Chen, Shun 
                AU  - Zhu, Dekang 
                AU  - Liu, Mafeng 
                AU  - Zhao, Xinxin 
                AU  - Yang, Qiao 
                AU  - Wu, Ying 
                AU  - Huang, Juan 
                AU  - Zhang, Shaqiu 
                AU  - Mao, Sai 
                AU  - Ou, Xumin 
                AU  - Gao, Qun 
                AU  - Yu, Yanling 
                AU  - Liu, Yunya 
                AU  - Zhang, Ling 
                AU  - Yin, Zhongqiong 
                AU  - Jing, Bo 
                AU  - Tian, Bin 
                AU  - Pan, Leichang 
                AU  - Rehman, Mujeeb Ur 
                AU  - Chen, Xiaoyue 
                AU  - Jia, Renyong 
                TI  - Transcriptome analysis of duck embryo fibroblasts for the dynamic response to duck tembusu virus infection and dual regulation of apoptosis genes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103759
                DO  - 10.18632/aging.103759
                SP  - 17503
                EP  - 17527
                PY  - 
                AB  - Duck Tembusu virus (DTMUV) is an emerging pathogenic flavivirus that has caused enormous economic losses in Southeast Asia. However, the pathogenic mechanism and host&#x2019;s responses after DTMUV infection remain poorly understood. During this study, total mRNA sequencing (RNA-Seq) analysis was used to detect the global gene expression in DEFs at various time points after DTMUV infection. We identified 326 genes altered significantly at all time points, and these genes were dynamically enriched in multifarious biological processes, including apoptosis, innate immune response, DNA replication, cell cycle arrest and DNA repair. Next, the results showed that apoptosis was induced and the proportion of apoptosis increased with time, and pro-apoptotic molecules caspases were activated. The RNA-seq data analysis further revealed that most pro-apoptosis and anti-apoptosis genes were early continually responsive, and the genes involved in both intrinsic and extrinsic apoptotic pathways were initiated. Further, the considerably enriched immune-relevant pathways were involved in apoptosis process, and protein-protein interactions (PPIs) analysis showed that IL6, STAT1, TNFAIP3, CFLAR and PTGS2 may be key regulators of DEFs apoptosis. In conclusion, this study not only contributes to understanding the underlying mechanism of DEFs infection with DTMUV, but also provides new insights into targets screening for antiviral therapy.
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Two identified subsets of CD8 T cells in obstructed kidneys play different roles in inflammation and fibrosis

Juan Wang, Jijing Tian, Jian Sun, Min Gao, Yanjun Dong,

https://doi.org/10.18632/aging.103764 pp 17528—17540

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Wang J, Tian J, Sun J, Gao M, Dong Y, . Two identified subsets of CD8 T cells in obstructed kidneys play different roles in inflammation and fibrosis. . 12:17528-17540. https://doi.org/10.18632/aging.103764

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                TY  - JOUR
                AU  - Wang, Juan 
                AU  - Tian, Jijing 
                AU  - Sun, Jian 
                AU  - Gao, Min 
                AU  - Dong, Yanjun 
                TI  - Two identified subsets of CD8 T cells in obstructed kidneys play different roles in inflammation and fibrosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103764
                DO  - 10.18632/aging.103764
                SP  - 17528
                EP  - 17540
                PY  - 
                AB  - Inflammation plays a crucial role in initiating renal fibrosis after injury. The infiltration of inflammatory cells, such as CD4+ T cells and macrophages, contributes to renal fibrosis following ureteric obstruction. However, the function of CD8+ T cells in obstructed kidneys remains unclear. Although CD8+ T cell depletion intensifies renal fibrosis by decreasing IFN-&#x3B3; and increasing IL-4 in the kidneys, the change and role of CD8 T cell populations following environmental changes during renal fibrosis are largely unknown. Here, we identified two CD8 T cell subsets in mouse obstructed kidneys with unilateral ureteric obstruction and revealed their different functions in building an inflammatory or profibrotic environment. Following renal fibrosis, the phenotypes of infiltrated CD8 T cells were mainly Tc1 (CD44+CD25&#x2212;CD62L&#x2212;) at the early inflammation stage and then changed to Tc2 (CD44+CD25highCD62Llow). Tc1 and Tc2 secreted IFN-&#x3B3;, contributing to the decrease in the Th2-induced over-polarization of M2 macrophages and fibrosis. Moreover, Tc2 secreted pro- and anti-inflammation factors and decreased the inflammatory responses of other cells to control inflammation and fibrosis. This work and our previous study showed that CD8 T cells could balance out inflammation by controlling its level in renal fibrosis.
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BRD4/8/9 are prognostic biomarkers and associated with immune infiltrates in hepatocellular carcinoma

Yi-Ru Chen, Su-Shan Ouyang, Yan-Ling Chen, Ping Li, Hui-Wen Xu, Sen-Lin Zhu,

https://doi.org/10.18632/aging.103768 pp 17541—17567

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Chen Y, Ouyang S, Chen Y, Li P, Xu H, Zhu S, . BRD4/8/9 are prognostic biomarkers and associated with immune infiltrates in hepatocellular carcinoma. . 12:17541-17567. https://doi.org/10.18632/aging.103768

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                TY  - JOUR
                AU  - Chen, Yi-Ru 
                AU  - Ouyang, Su-Shan 
                AU  - Chen, Yan-Ling 
                AU  - Li, Ping 
                AU  - Xu, Hui-Wen 
                AU  - Zhu, Sen-Lin 
                TI  - BRD4/8/9 are prognostic biomarkers and associated with immune infiltrates in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103768
                DO  - 10.18632/aging.103768
                SP  - 17541
                EP  - 17567
                PY  - 
                AB  - Bromodomain (BRD)-containing proteins are a class of epigenetic readers with unique recognition for N-acetyl-lysine in histones and functions of gene transcription and chromatin modification, known to be critical in various cancers. However, little is known about the roles of distinct BRD-containing protein genes in hepatocellular carcinoma (HCC). Most recently, we investigated the transcriptional and survival data of BRD1, BRD2, BRD3, BRD4, BRD7, BRD8, BRD9 in HCC patients through ONCOMINE, UALCAN, Human Protein Atlas, GEPIA, cBioPortal, STRING, TIMER databases. BRD1/2/3/4/7/8/9 were over-expressed in HCC and were significantly associated with clinical cancer stages and pathological tumor grades. High mRNA expressions of BRD4/8/9 were promising candidate biomarkers in HCC patients. The rate of sequence alternations in BRD1/2/3/4/7/8/9 was relatively high (52%) in HCC patients, and the genetic alternations were correlated with shorter overall survival and disease-free survival in HCC patients. Additionally, the mRNA expression levels of individual BRD genes were significantly positively associated with the immune infiltrating levels of B cells, CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells. And the associations between BRD1/2/3/4/7/8/9 and diverse immune marker sets showed a significance. Overall, these results indicated that BRD4/8/9 could be potential prognostic markers and druggable epigenetic targets in HCC patients.
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HSPB8 overexpression prevents disruption of blood-brain barrier after intracerebral hemorrhage in rats through Akt/GSK3β/β-catenin signaling pathway

Ying Hou, Zhiping Hu, Xiyu Gong, Binbin Yang,

https://doi.org/10.18632/aging.103773 pp 17568—17581

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Hou Y, Hu Z, Gong X, Yang B, . HSPB8 overexpression prevents disruption of blood-brain barrier after intracerebral hemorrhage in rats through Akt/GSK3β/β-catenin signaling pathway. . 12:17568-17581. https://doi.org/10.18632/aging.103773

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                TY  - JOUR
                AU  - Hou, Ying 
                AU  - Hu, Zhiping 
                AU  - Gong, Xiyu 
                AU  - Yang, Binbin 
                TI  - HSPB8 overexpression prevents disruption of blood-brain barrier after intracerebral hemorrhage in rats through Akt/GSK3β/β-catenin signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103773
                DO  - 10.18632/aging.103773
                SP  - 17568
                EP  - 17581
                PY  - 
                AB  - Blood brain barrier (BBB) disruption is a crucial factor contributing to secondary brain injury after intracerebral hemorrhage (ICH). Heat shock protein B8 (HSPB8) has been recently reported to confer neuroprotection against against ischaemic stroke through maintaining BBB integrity. However, the role of HSPB8 in ICH is still elusive. In this study, we found that HSPB8 was upregulated by ICH and extensively expressed in neurovascular structure including endothelial cells and astrocytes. lentivirus intracerebroventricular (i.c.v) injection achieved a widespread and persistent HSPB8 overexpression in brain tissues. HSPB8 overexpression significantly ameliorated neurobehavioral deficits and brain edema at 24 and 72h following ICH. Moreover, HSPB8 overexpression remarkedly inhibited BBB disruption and significantly increase the level of p-Akt, p-GSK&#x3B2; and intranuclear &#x3B2;-catenin 24h post-ICH. This effect was obviously reversed by Akt specific inhibitor, MK2206. Based on these findings, HSPB8 exerted its protective effect on BBB, at least partly, via Akt/ p-GSK&#x3B2;/&#x3B2;-catenin pathways.
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Metformin suppresses Nrf2-mediated chemoresistance in hepatocellular carcinoma cells by increasing glycolysis

Liangyu Cai, Xin Jin, Jiannan Zhang, Le Li, Jinfeng Zhao,

https://doi.org/10.18632/aging.103777 pp 17582—17600

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Cai L, Jin X, Zhang J, Li L, Zhao J, . Metformin suppresses Nrf2-mediated chemoresistance in hepatocellular carcinoma cells by increasing glycolysis. . 12:17582-17600. https://doi.org/10.18632/aging.103777

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                TY  - JOUR
                AU  - Cai, Liangyu 
                AU  - Jin, Xin 
                AU  - Zhang, Jiannan 
                AU  - Li, Le 
                AU  - Zhao, Jinfeng 
                TI  - Metformin suppresses Nrf2-mediated chemoresistance in hepatocellular carcinoma cells by increasing glycolysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103777
                DO  - 10.18632/aging.103777
                SP  - 17582
                EP  - 17600
                PY  - 
                AB  - The diabetes drug metformin has recently been shown to possess anti-cancer properties when used with other chemotherapeutic drugs. However, detailed mechanisms by which metformin improves cancer treatment are poorly understood. Here we provide evidence in HepG2 hepatocellular carcinoma cells that metformin sensitizes cisplatin-resistant HepG2 cells (HepG2/DDP) through increasing cellular glycolysis and suppressing Nrf2-dependent transcription. We show that metformin increases glucose uptake and enhances glucose metabolism through glycolytic pathway, resulting in elevated concentrations of intracellular NADPH and lactate. Consistently, high glucose medium suppresses Nrf2-dependent transcription and sensitizes HepG2/DDP cells to cisplatin. Elevated glycolysis was required for metformin to regulate Nrf2-dependent transcription and cisplatin sensitivity, as inhibition of glycolysis with 2-Deoxy-D-glucose (2-DG) significantly mitigates the beneficial effect of metformin. Together, our study has revealed an important biological process and gene transcriptional program underlying the beneficial effect of metformin on reducing chemo-resistance in HepG2 cells and provided new information on improving chemotherapy of liver cancers.
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Parietal epithelial cell differentiation to a podocyte fate in the aged mouse kidney

Natalya V. Kaverina, Diana G. Eng, Jeffrey H. Miner, Jeffrey W. Pippin, Stuart J. Shankland,

https://doi.org/10.18632/aging.103788 pp 17601—17624

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Kaverina NV, Eng DG, Miner JH, Pippin JW, Shankland SJ, . Parietal epithelial cell differentiation to a podocyte fate in the aged mouse kidney. . 12:17601-17624. https://doi.org/10.18632/aging.103788

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                TY  - JOUR
                AU  - Kaverina, Natalya V. 
                AU  - Eng, Diana G. 
                AU  - Miner, Jeffrey H. 
                AU  - Pippin, Jeffrey W. 
                AU  - Shankland, Stuart J. 
                TI  - Parietal epithelial cell differentiation to a podocyte fate in the aged mouse kidney
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103788
                DO  - 10.18632/aging.103788
                SP  - 17601
                EP  - 17624
                PY  - 
                AB  - Healthy aging is typified by a progressive and absolute loss of podocytes over the lifespan of animals and humans. To test the hypothesis that a subset of glomerular parietal epithelial cell (PEC) progenitors transition to a podocyte fate with aging, dual reporter PEC-rtTA|LC1|tdTomato|Nphs1-FLPo|FRT-EGFP mice were generated. PECs were inducibly labeled with a tdTomato reporter, and podocytes were constitutively labeled with an EGFP reporter. With advancing age (14 and 24 months) glomeruli in the juxta-medullary cortex (JMC) were more severely injured than those in the outer cortex (OC). In aged mice (24m), injured glomeruli with lower podocyte number (41% decrease), showed more PEC migration and differentiation to a podocyte fate than mildly injured or healthy glomeruli. PECs differentiated to a podocyte fate had ultrastructural features of podocytes and co-expressed the podocyte markers podocin, nephrin, p57 and VEGF164, but not markers of mesangial (Perlecan) or endothelial (ERG) cells. PECs differentiated to a podocyte fate did not express CD44, a marker of PEC activation. Taken together, we demonstrate that a subpopulation of PECs differentiate to a podocyte fate predominantly in injured glomeruli in mice of advanced age.
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Graphene oxide inhibits cell migration and invasion by destroying actin cytoskeleton in cervical cancer cells

Jing Wang, Ping Wang, Ying He, Xiaoli Liu, Sisi Wang, Chunxing Ma, Xiaofei Tian, Jing Wang, Xin Wu,

https://doi.org/10.18632/aging.103821 pp 17625—17633

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Wang J, Wang P, He Y, Liu X, Wang S, Ma C, Tian X, Wang J, Wu X, . Graphene oxide inhibits cell migration and invasion by destroying actin cytoskeleton in cervical cancer cells. . 12:17625-17633. https://doi.org/10.18632/aging.103821

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                TY  - JOUR
                AU  - Wang, Jing 
                AU  - Wang, Ping 
                AU  - He, Ying 
                AU  - Liu, Xiaoli 
                AU  - Wang, Sisi 
                AU  - Ma, Chunxing 
                AU  - Tian, Xiaofei 
                AU  - Wang, Jing 
                AU  - Wu, Xin 
                TI  - Graphene oxide inhibits cell migration and invasion by destroying actin cytoskeleton in cervical cancer cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103821
                DO  - 10.18632/aging.103821
                SP  - 17625
                EP  - 17633
                PY  - 
                AB  - Objective: To investigate the antitumor effects of Graphene oxide (GO) on tumor invasion and metastasis in human cervical cancer Hela cells.Results: GO significantly inhibited cell viability and the number of clones, promoted cell apoptosis, as well as suppressed cell migration and invasion, and destroyed the structure of actin cytoskeleton of Hela cells in a dose-dependent manner in. Moreover, the expression of metastasis-related proteins, including MMP2 and Cdc42, were significantly suppressed by the treatment of GO. And the expression of MMP3 was remarkably increased by Smad inhibitor and the protein levels of MMP3 and ICAM were elevated by the JNK inhibitor in GO-treated Hela cells.Conclusion: GO exhibited inhibitory effects on cell migration and invasion possibly by destroying actin cytoskeleton in Hela cells, which is a potential component of the Smad and JNK signalling pathways.Methods: GO was prepared and chracterized by UV visible light absorption spectroscopy and atomic force microscopy. Hela cells were treated with Go at different dose levels. Then, in vitro cytotoxicity of GO was evaluated by the MTT assay, colony-forming assay and cell apoptosis assay. The inhibitory effects of GO on tumor cell migration and invasion as well as actin cytoskeleton were explored using Hela cells.
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DUSP4 directly deubiquitinates and stabilizes Smad4 protein, promoting proliferation and metastasis of colorectal cancer cells

Weifeng Xu, Beibei Chen, Dianshan Ke, Xiaobing Chen,

https://doi.org/10.18632/aging.103823 pp 17634—17646

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Xu W, Chen B, Ke D, Chen X, . DUSP4 directly deubiquitinates and stabilizes Smad4 protein, promoting proliferation and metastasis of colorectal cancer cells. . 12:17634-17646. https://doi.org/10.18632/aging.103823

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                TY  - JOUR
                AU  - Xu, Weifeng 
                AU  - Chen, Beibei 
                AU  - Ke, Dianshan 
                AU  - Chen, Xiaobing 
                TI  - DUSP4 directly deubiquitinates and stabilizes Smad4 protein, promoting proliferation and metastasis of colorectal cancer cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103823
                DO  - 10.18632/aging.103823
                SP  - 17634
                EP  - 17646
                PY  - 
                AB  - Colorectal cancer is a common health-threatening tumor within the gastrointestinal tract. The aim of this study was to test the biological role of DUSP4 in colorectal cancer cells. In our study, DUSP4 overexpression-treated HCT116 cells and DUSP4 knockdown-treated SW480 cells were selected to perform study. Quantitative real-time PCR test (qRT-PCR) and western blot were used to detect DUSP4 abundance in clinical tissues and six cell lines, as well as ubiquitin-related Smad4 degradation. Western blot, migration and invasion. were used to assess the relationships between DUSP4 and Smad4. Higher DUSP4 expression of functional significance was observed in colorectal cancer tissues and cells. The results showed that both treatments could affect the proliferation, colony formation, migration, invasion of tumor cells, and the expression of epithelial mesenchymal transformation (EMT)-associated biomarkers. Moreover, in colorectal cancer cells, DUSP4 could promote the Smad4 degradation by regulating ubiquitin-related Smad4 degradation, and promote the cell proliferation, migration and invasion by regulating Smad4 degradation via Smad4 gene. Meanwhile, DUSP4 can directly deubiquitinate and stabilize Smad4 protein, hence further promote proliferation and metastasis of colorectal cancer cells.
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Identification and prognostic value of metabolism-related genes in gastric cancer

Fang Wen, Jiani Huang, Xiaona Lu, Wenjie Huang, Yulan Wang, Yingfeng Bai, Shuai Ruan, Suping Gu, Xiaoxue Chen, Peng Shu,

https://doi.org/10.18632/aging.103838 pp 17647—17661

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Wen F, Huang J, Lu X, Huang W, Wang Y, Bai Y, Ruan S, Gu S, Chen X, Shu P, . Identification and prognostic value of metabolism-related genes in gastric cancer. . 12:17647-17661. https://doi.org/10.18632/aging.103838

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                TY  - JOUR
                AU  - Wen, Fang 
                AU  - Huang, Jiani 
                AU  - Lu, Xiaona 
                AU  - Huang, Wenjie 
                AU  - Wang, Yulan 
                AU  - Bai, Yingfeng 
                AU  - Ruan, Shuai 
                AU  - Gu, Suping 
                AU  - Chen, Xiaoxue 
                AU  - Shu, Peng 
                TI  - Identification and prognostic value of metabolism-related genes in gastric cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103838
                DO  - 10.18632/aging.103838
                SP  - 17647
                EP  - 17661
                PY  - 
                AB  - Gastric cancer (GC) is one of the most commonly occurring cancers, and metabolism-related genes (MRGs) are associated with its development. Transcriptome data and the relevant clinical data were downloaded from The Cancer Genome Atlas and Gene Expression Omnibus databases, and we identified 194 MRGs differentially expressed between GC and adjacent nontumor tissues. Through univariate Cox and lasso regression analyses we identified 13 potential prognostic differentially expressed MRGs (PDEMRGs). These PDEMRGs (CKMT2, ME1, GSTA2, ASAH1, GGT5, RDH12, NNMT, POLR1A, ACYP1, GLA, OPLAH, DCK, and POLD3) were used to build a Cox regression risk model to predict the prognosis of GC patients. Further univariate and multivariate Cox regression analyses showed that this model could serve as an independent prognostic parameter. Gene Set Enrichment Analysis showed significant enrichment pathways that could potentially contribute to pathogenesis. This model also revealed the probability of genetic alterations of PDEMRGs. We have thus identified a valuable metabolic model for predicting the prognosis of GC patients. The PDEMRGs in this model reflect the dysregulated metabolic microenvironment of GC and provide useful noninvasive biomarkers.
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Shikonin overcomes drug resistance and induces necroptosis by regulating the miR-92a-1-5p/MLKL axis in chronic myeloid leukemia

Xianbo Huang, Zhenzhen Chen, Fan Ni, Xiujin Ye, Wenbin Qian,

https://doi.org/10.18632/aging.103844 pp 17662—17680

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Huang X, Chen Z, Ni F, Ye X, Qian W, . Shikonin overcomes drug resistance and induces necroptosis by regulating the miR-92a-1-5p/MLKL axis in chronic myeloid leukemia. . 12:17662-17680. https://doi.org/10.18632/aging.103844

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                TY  - JOUR
                AU  - Huang, Xianbo 
                AU  - Chen, Zhenzhen 
                AU  - Ni, Fan 
                AU  - Ye, Xiujin 
                AU  - Qian, Wenbin 
                TI  - Shikonin overcomes drug resistance and induces necroptosis by regulating the miR-92a-1-5p/MLKL axis in chronic myeloid leukemia
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103844
                DO  - 10.18632/aging.103844
                SP  - 17662
                EP  - 17680
                PY  - 
                AB  - Development of resistance to tyrosine kinase inhibitors (TKIs) targeting the BCR/ABL fusion protein represents a major challenge in the treatment of chronic myeloid leukemia (CML). Since apoptosis resistance is the fundamental mechanism impeding TKIs&#x2019; therapeutic effects, alternative approaches that induce nonapoptotic cell death are being pursued to treat TKI-resistant CML. Induction of necroptosis, a distinct, caspase-independent form of programmed cell death, may be a valuable strategy in this respect. The present study shows that shikonin, an herbal compound used in traditional Chinese medicine, overcomes TKI resistance in BCR/ABL-positive CML cells by inducing necroptosis via activation of RIPK1/RIPK3/MLKL signaling. This effect occurs both in vitro and in vivo and involves downregulation of miR-92a-1-5p, a poor-prognosis marker frequently overexpressed in leukemia patients. Based on gene expression experiments, we conclude that miR-92a-1-5p promotes CML progression by inhibiting MLKL expression. Accordingly, we show that antagomiR-mediated in vivo inhibition of miR-92a-1-5p reduces the growth of CML tumors in mice through necroptosis induction. Our research suggests that therapies that relieve MLKL suppression by targeting miR-92a-1-5p may represent a useful strategy to treat TKI-refractory CML.
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Long non-coding RNA Loc490 inhibits gastric cancer cell proliferation and metastasis by upregulating RNA-binding protein Quaking

Zhengxi He, Zhaojun Duan, Ling Chen, Bin Li, Yanhong Zhou,

https://doi.org/10.18632/aging.103876 pp 17681—17693

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He Z, Duan Z, Chen L, Li B, Zhou Y, . Long non-coding RNA Loc490 inhibits gastric cancer cell proliferation and metastasis by upregulating RNA-binding protein Quaking. . 12:17681-17693. https://doi.org/10.18632/aging.103876

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                TY  - JOUR
                AU  - He, Zhengxi 
                AU  - Duan, Zhaojun 
                AU  - Chen, Ling 
                AU  - Li, Bin 
                AU  - Zhou, Yanhong 
                TI  - Long non-coding RNA Loc490 inhibits gastric cancer cell proliferation and metastasis by upregulating RNA-binding protein Quaking
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103876
                DO  - 10.18632/aging.103876
                SP  - 17681
                EP  - 17693
                PY  - 
                AB  - Gastric cancer (GC) is one of the most common malignant tumor types worldwide. Long non-coding RNAs (lncRNAs) have important epigenetic effects, including altering the proliferation and metastasis of malignant tumors. We used gene chip technology to search for lncRNAs that were differentially expressed in GC and metastatic lymph node tissues compared with adjacent normal tissues. The lncRNA Loc490 and the RNA-binding protein Quaking (QKI) were downregulated in GC tissues and lymph node metastases compared with normal tissues, and the levels of these two genes correlated positively with one another. Loc490 expression correlated negatively with lymph node metastasis and vein/nerve invasion, while it correlated positively with overall and disease-free survival. In vitro, Loc490 post-translationally enhanced the expression of QKI and suppressed the expression of epithelial-mesenchymal transition-related molecules. Overexpression of Loc490 inhibited GC cell proliferation, invasion and metastasis and exerted strong antitumor effects in vivo, while silencing of QKI antagonized these effects. A potential binding site between Loc490 and QKI was detected through bioinformatics analysis and confirmed through RNA immunoprecipitation and mutant analyses. Our results suggest that lncRNA Loc490 inhibits GC cell proliferation and metastasis by upregulating RNA-binding protein QKI.
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Preclinical studies show using enzalutamide is less effective in docetaxel-pretreated than in docetaxel-naïve prostate cancer cells

Changyi Lin, Fu-Ju Chou, Jieyang Lu, Wanying Lin, Matthew Truong, Hao Tian, Yin Sun, Jie Luo, Rachel Yang, Yuanjie Niu, Rosa Nadal, Emmanuel S. Antonarakis, Carlos Cordon-Cardo, Deepak Sahasrabudhe, Chi-Ping Huang, Shuyuan Yeh, Gonghui Li, Chawnshang Chang,

https://doi.org/10.18632/aging.103917 pp 17694—17712

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Lin C, Chou F, Lu J, Lin W, Truong M, Tian H, Sun Y, Luo J, Yang R, Niu Y, Nadal R, Antonarakis ES, Cordon-Cardo C, et al, . Preclinical studies show using enzalutamide is less effective in docetaxel-pretreated than in docetaxel-naïve prostate cancer cells. . 12:17694-17712. https://doi.org/10.18632/aging.103917

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                TY  - JOUR
                AU  - Lin, Changyi 
                AU  - Chou, Fu-Ju 
                AU  - Lu, Jieyang 
                AU  - Lin, Wanying 
                AU  - Truong, Matthew 
                AU  - Tian, Hao 
                AU  - Sun, Yin 
                AU  - Luo, Jie 
                AU  - Yang, Rachel 
                AU  - Niu, Yuanjie 
                AU  - Nadal, Rosa 
                AU  - Antonarakis, Emmanuel S. 
                AU  - Cordon-Cardo, Carlos 
                AU  - Sahasrabudhe, Deepak 
                AU  - Huang, Chi-Ping 
                AU  - Yeh, Shuyuan 
                AU  - Li, Gonghui 
                AU  - Chang, Chawnshang 
                TI  - Preclinical studies show using enzalutamide is less effective in docetaxel-pretreated than in docetaxel-naïve prostate cancer cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103917
                DO  - 10.18632/aging.103917
                SP  - 17694
                EP  - 17712
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Lin, Changyi 
                AU  - Chou, Fu-Ju 
                AU  - Lu, Jieyang 
                AU  - Lin, Wanying 
                AU  - Truong, Matthew 
                AU  - Tian, Hao 
                AU  - Sun, Yin 
                AU  - Luo, Jie 
                AU  - Yang, Rachel 
                AU  - Niu, Yuanjie 
                AU  - Nadal, Rosa 
                AU  - Antonarakis, Emmanuel S. 
                AU  - Cordon-Cardo, Carlos 
                AU  - Sahasrabudhe, Deepak 
                AU  - Huang, Chi-Ping 
                AU  - Yeh, Shuyuan 
                AU  - Li, Gonghui 
                AU  - Chang, Chawnshang 
                TI  - Preclinical studies show using enzalutamide is less effective in docetaxel-pretreated than in docetaxel-naïve prostate cancer cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103917
                DO  - 10.18632/aging.103917
                SP  - 17694
                EP  - 17712
                PY  - 
                AB  - Anti-androgen therapy with Enzalutamide (Enz) has been used as a therapy for castration resistant prostate cancer (CRPC) patients after development of resistance to chemotherapy with Docetaxel (Doc). The potential impacts of Doc-chemotherapy on the subsequent Enz treatment, however, remain unclear. Here we found the overall survival rate of patients that received Enz was significantly less in patients that received prior Doc-chemotherapy than those who had not. In vitro studies from 3 established Doc resistant CRPC (DocRPC) cell lines are consistent with the clinical findings showing DocRPC patients had decreased Enz-sensitivity as well as accelerated development of Enz-resistance via enhanced androgen receptor (AR) splicing variant 7 (ARv7) expression. Mechanism dissection found that Doc treatment might increase the generation of ARv7 via altering the MALAT1-SF2 RNA splicing complex. Preclinical studies using in vivo mouse models and in vitro cell lines proved that targeting the MALAT1/SF2/ARv7 axis with small molecules, including siMALAT1, shSF2, and shARv7 or ARv7 degradation enhancers: Cisplatin or ASC-J9&#xAE;, can restore/increase the Enz sensitivity to further suppress DocRPC cell growth. Therefore, combined therapy of Doc-chemotherapy with anti-ARv7 therapy, including Cisplatin or ASC-J9&#xAE;, may be developed to increase the efficacy of Enz to further suppress DocRPC in patients.
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Sex specific inflammatory profiles of cerebellar mitochondria are attenuated in Parkinson’s disease

Thomas L. Ingram, Freya Shephard, Sarir Sarmad, Catherine A. Ortori, David A. Barrett, Lisa Chakrabarti,

https://doi.org/10.18632/aging.103937 pp 17713—17737

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Ingram TL, Shephard F, Sarmad S, Ortori CA, Barrett DA, Chakrabarti L, . Sex specific inflammatory profiles of cerebellar mitochondria are attenuated in Parkinson’s disease. . 12:17713-17737. https://doi.org/10.18632/aging.103937

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                TY  - JOUR
                AU  - Ingram, Thomas L. 
                AU  - Shephard, Freya 
                AU  - Sarmad, Sarir 
                AU  - Ortori, Catherine A. 
                AU  - Barrett, David A. 
                AU  - Chakrabarti, Lisa 
                TI  - Sex specific inflammatory profiles of cerebellar mitochondria are attenuated in Parkinson’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 17
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103937
                DO  - 10.18632/aging.103937
                SP  - 17713
                EP  - 17737
                PY  - 
                AB  - Response to inflammation is a key determinant in many diseases and their outcomes. Diseases that commonly affect older people are frequently associated with altered inflammatory processes. Neuroinflammation has been described in Parkinson&apos;s disease (PD) brain. PD is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta and at the sub-cellular level, mitochondrial dysfunction is a key feature. However, there is evidence that a different region of the brain, the cerebellum, is involved in the pathophysiology of PD. We report relative levels of 40 pro- and anti-inflammatory cytokines measured in PD and control cerebellar mitochondria. These data were obtained by screening cytokine antibody arrays. In parallel, we present concentrations of 29 oxylipins and 4 endocannabinoids measured in mitochondrial fractions isolated from post-mortem PD cerebellum with age and sex matched controls. Our oxylipin and endocannabinoid data were acquired via quantitation by LC-ESI&#x2014;MS/MS. The separate sample sets both show there are clearly different inflammatory profiles between the sexes in control samples. Sex specific profiles were not maintained in cerebellar mitochondria isolated from PD brains.
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Anti-aging effects of Ribes meyeri anthocyanins on neural stem cells and aging mice

Jiaming Gao, Yating Wu, Dajun He, Xiaoqi Zhu, Hongbin Li, Haifeng Liu, Hailiang Liu,

https://doi.org/10.18632/aging.103955 pp 17738—17753

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Gao J, Wu Y, He D, Zhu X, Li H, Liu H, Liu H, . Anti-aging effects of Ribes meyeri anthocyanins on neural stem cells and aging mice. . 12:17738-17753. https://doi.org/10.18632/aging.103955

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 TY - JOUR
 AU - Gao, Jiaming 
 AU - Wu, Yating 
 AU - He, Dajun 
 AU - Zhu, Xiaoqi 
 AU - Li, Hongbin 
 AU - Liu, Haifeng 
 AU - Liu, Hailiang 
 TI - Anti-aging effects of Ribes meyeri anthocyanins on neural stem cells and aging mice
 JO - 
 JA - 
 VL - 12
 IS - 17
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103955
 DO - 10.18632/aging.103955
 SP - 17738
 EP - 17753
 PY - 
 AB - Aging is associated with neurological impairment and cognitive decline. Flavonoids are very promising in anti-aging research in mouse models. Ribes meyeri anthocyanins are rich in abundant flavonoids, but their anti-aging biological activities remain unknown. In this study, we prepared an R. meyeri anthocyanin extract and analyzed its effects on neural stem cell (NSC) senescence in vivo and in vitro. We isolated mouse NSCs and used cell counting kit-8 (CCK-8), cell cycle, reactive oxygen species (ROS), and immunofluorescence methods to analyze the anti-aging effects of R. meyeri anthocyanins as well as naringenin (Nar), which metabolic analysis revealed as an important flavonoid in R. meyeri anthocyanins. RNA-sequencing (RNA-seq) and enzyme-linked immuno sorbent assay (ELISA) methods were also used to investigate Nar-specific mechanisms of anti-aging. After R. meyeri anthocyanin treatment, NSC proliferation accelerated, and NSCs had decreased senescence markers, and reduced P16ink4a expression. R. meyeri anthocyanin treatment also reversed age-dependent neuronal loss in vivo and in vitro. Nar blocked mNSC aging in vitro and improved spatial memory and cognitive abilities in aging mice through downregulation of plasma TNF-&#x3B1; protein. These findings suggest that R. meyeri anthocyanins increase NSC proliferation and improve neurogenesis with aging via Nar-induced reductions in TNF-&#x3B1; protein levels in vivo.
 ER -

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Volume 12, Issue 17

About the Cover

Editorials

Shuai Jiang,

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Qihua Tan,

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Thomas H. Ambrosi, L. Henry Goodnough, Charles K.F. Chan,

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Letter to the Editor

COVID-19 A newborn with normal IgM and elevated IgG antibodies born to an asymptomatic infection mother with COVID-19

Wenqi Gao, Zhifang Deng, Lingkong Zeng, Yuan Yang, HongJian Gong, Jue Liu, Han Xiao,

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Research Papers

COVID-19 Clinical course and risk factors for recurrence of positive SARS-CoV-2 RNA: a retrospective cohort study from Wuhan, China

Jie Chen, Xiaoping Xu, Jing Hu, Qiangda Chen, Fengfeng Xu, Hui Liang, Nanmei Liu, Hengmei Zhu, Jinlong Lan, Lan Zhou, Jiajun Xing, Ning Pu, Zhigang Cai,

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Kiyana Zarnani, Stephen M. Smith, Fidel Alfaro-Almagro, Birgitte Fagerlund, Martin Lauritzen, Egill Rostrup, Thomas E. Nichols,

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Dana Hashim, Greta Carioli, Matteo Malvezzi, Paola Bertuccio, Samuel Waxman, Eva Negri, Carlo La Vecchia, Paolo Boffetta,

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Feiteng Huang, Jie Sun, Wei Chen, Xin He, Yinghui Zhu, Haojie Dong, Hanying Wang, Zheng Li, Lei Zhang, Samer Khaled, Guido Marcucci, Jinwen Huang, Ling Li,

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Li Zhang, Chen Bai, Chao Nie, Xiaoquan Zhu, Huiping Yuan, Liang Sun, Qi Zhou, Xiaoling Li, Xuan Xian, Fan Yang, Guofang Pang, Yuan Lv, Xiaolin Ni, Caiyou Hu, Ze Yang,

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Yu-Che Cheng, Wei-Chi Ku, Ting-Ting Tseng, Ching-Po Wu, Mengjin Li, Shao-Chen Lee,

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Rongjun Wan, Juan Jiang, Chengping Hu, Xi Chen, Cen Chen, Bingrong Zhao, Xinyue Hu, Zhiyuan Zheng, Yuanyuan Li,

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Juntao Li, Yan Zhou, Yuting Yan, Zhongnan Zheng, Yabin Hu, Wei Wu,

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Xin Yang, Mohan Zhang, Yuhua Dai, Yuchao Sun, Yahyah Aman, Yuying Xu, Peilin Yu, Yifan Zheng, Jun Yang, Xinqiang Zhu,

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Zhijie Jian, Hongrui Guo, Huan Liu, Hengmin Cui, Jing Fang, Zhicai Zuo, Junliang Deng, Yinglun Li, Xun Wang, Ling Zhao,

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Li Li, Bing Wang, Yawei Li, Lei Li, Yuliang Dai, Guohua Lv, Pengfei Wu, Pengzhi Li,

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Xing-Hua Pan, Qing-Keng Lin, Xiang Yao, Zi-An Li, Xue-Min Cai, Rong-Qing Pang, Guang-Ping Ruan,

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Miao Li, John Simon Alsager, Zhaokai Wang, Lin Cheng, Bin Shan,

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Dabing Huang, Xianhai Zhu, Yong Wang, Haobin Yu, Youguang Pu,

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COVID-19
A newborn with normal IgM and elevated IgG antibodies born to an asymptomatic infection mother with COVID-19

COVID-19
Clinical course and risk factors for recurrence of positive SARS-CoV-2 RNA: a retrospective cohort study from Wuhan, China