Volume 11, Issue 15

Yu L, Gui S, Liu Y, Qiu X, Zhang G, Zhang X, Pan J, Fan J, Qi S, Qiu B, . Exosomes derived from microRNA-199a-overexpressing mesenchymal stem cells inhibit glioma progression by down-regulating AGAP2. . 11:5300-5318. https://doi.org/10.18632/aging.102092

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                TY  - JOUR
                AU  - Yu, Lei 
                AU  - Gui, Si 
                AU  - Liu, Yawei 
                AU  - Qiu, Xiaoyu 
                AU  - Zhang, Guozhong 
                AU  - Zhang, Xi’an 
                AU  - Pan, Jun 
                AU  - Fan, Jun 
                AU  - Qi, Songtao 
                AU  - Qiu, Binghui 
                TI  - Exosomes derived from microRNA-199a-overexpressing mesenchymal stem cells inhibit glioma progression by down-regulating AGAP2
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102092
                DO  - 10.18632/aging.102092
                SP  - 5300
                EP  - 5318
                PY  - 
                AB  - Accumulating evidence has implied that microRNAs (miRNAs) are implicated in glioma progression, and genetically engineered mesenchymal stem cells can help to inhibit tumor growth of glioma. Herein we hypothesized that miR-199a could be delivered by mesenchymal stem cells to glioma cells through exosomes and thus prevent the glioma development by down-regulating ArfGAP with GTPase domain, ankyrin repeat and PH domain 2 (AGAP2). The expression pattern of miR-199a and AGAP2 was characterized in glioma tissues and cells using RNA polymerase chain reaction quantification, immunohistochemical staining and Western blot assays. Mesenchymal stem cells transfected with miR-199a mimic or their derived exosomes were co-cultured with U251 cells. The biological behaviors as well as chemosensitivity of U251 cells were assessed to explore the involvement of miR-199a/AGAP2 in glioma. MiR-199a was poorly expressed in glioma tissue and cells while AGAP2 was highly expressed. Mesenchymal stem cells delivered miR-199a to the glioma cells via the exosomes, which resulted in the suppression of the proliferation, invasion and migration of glioma cells. Besides, mesenchymal stem cells over-expressing miR-199a enhanced the chemosensitivity to temozolomide and inhibited the tumor growth in vivo. Taken together, mesenchymal stem cell-derived exosomal miR-199a can inhibit the progression of glioma by down-regulating AGAP2.
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Association of basal metabolic rate and fuel oxidation in basal conditions and during exercise, with plasma S-klotho: the FIT-AGEING study

Francisco J. Amaro-Gahete, Alejandro De-la-O, Lucas Jurado-Fasoli, Jonatan R. Ruiz, Manuel J. Castillo,

https://doi.org/10.18632/aging.102100 pp 5319—5333

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Amaro-Gahete FJ, De-la-O A, Jurado-Fasoli L, Ruiz JR, Castillo MJ, . Association of basal metabolic rate and fuel oxidation in basal conditions and during exercise, with plasma S-klotho: the FIT-AGEING study. . 11:5319-5333. https://doi.org/10.18632/aging.102100

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                TY  - JOUR
                AU  - Amaro-Gahete, Francisco J. 
                AU  - De-la-O, Alejandro 
                AU  - Jurado-Fasoli, Lucas 
                AU  - Ruiz, Jonatan R. 
                AU  - Castillo, Manuel J. 
                TI  - Association of basal metabolic rate and fuel oxidation in basal conditions and during exercise, with plasma S-klotho: the FIT-AGEING study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102100
                DO  - 10.18632/aging.102100
                SP  - 5319
                EP  - 5333
                PY  - 
                AB  - S-klotho, the shed form of &#x3B1;-klotho, is thought to be an ageing suppressor with functions related to the physiology of energy metabolism. However, it remains unknown whether ageing biomarkers such as S-klotho and/or chronological ageing are associated in any way with basal metabolic rate (BMR) and fuel oxidation in basal conditions and during exercise. The present work investigates the association of BMR and fuel oxidation in basal conditions and during exercise, with plasma S-klotho in middle-aged, sedentary adults. BMR was measured by indirect calorimetry in 74 such subjects (53% women; age 53.7&#xB1;5.1 years) following standard procedures, and their fuel oxidation estimated via stoichiometric equations. The maximal fat oxidation during exercise (MFO) and the intensity of exercise that elicits MFO (Fatmax) were determined using a walking graded exercise test. No relationship was seen between BMR and plasma S-klotho (P&gt;0.1), although both basal fat oxidation and MFO showed positive associations with this protein (both P&lt;0.001); these relationships persisted after controlling for age, sex and fat mass. However, no significant associations were seen between BMR, basal fat oxidation or MFO and chronological age (all P&gt;0.1). The present findings suggest that basal fat oxidation and MFO are strongly associated with plasma S-klotho in middle-aged sedentary adults. These results support the idea that metabolic flexibility is a powerful predictor of biological ageing.
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Down-regulation of long non-coding RNA MEG3 suppresses osteogenic differentiation of periodontal ligament stem cells (PDLSCs) through miR-27a-3p/IGF1 axis in periodontitis

Yi Liu, Chunpeng Liu, Ankui Zhang, Shichang Yin, Ting Wang, Yan Wang, Meiming Wang, Yixin Liu, Qiaohui Ying, Jinrui Sun, Fulan Wei, Dongxu Liu, Chunling Wang, Shaohua Ge,

https://doi.org/10.18632/aging.102105 pp 5334—5350

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Liu Y, Liu C, Zhang A, Yin S, Wang T, Wang Y, Wang M, Liu Y, Ying Q, Sun J, Wei F, Liu D, Wang C, et al, . Down-regulation of long non-coding RNA MEG3 suppresses osteogenic differentiation of periodontal ligament stem cells (PDLSCs) through miR-27a-3p/IGF1 axis in periodontitis. . 11:5334-5350. https://doi.org/10.18632/aging.102105

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                TY  - JOUR
                AU  - Liu, Yi 
                AU  - Liu, Chunpeng 
                AU  - Zhang, Ankui 
                AU  - Yin, Shichang 
                AU  - Wang, Ting 
                AU  - Wang, Yan 
                AU  - Wang, Meiming 
                AU  - Liu, Yixin 
                AU  - Ying, Qiaohui 
                AU  - Sun, Jinrui 
                AU  - Wei, Fulan 
                AU  - Liu, Dongxu 
                AU  - Wang, Chunling 
                AU  - Ge, Shaohua 
                TI  - Down-regulation of long non-coding RNA MEG3 suppresses osteogenic differentiation of periodontal ligament stem cells (PDLSCs) through miR-27a-3p/IGF1 axis in periodontitis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102105
                DO  - 10.18632/aging.102105
                SP  - 5334
                EP  - 5350
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Liu, Yi 
                AU  - Liu, Chunpeng 
                AU  - Zhang, Ankui 
                AU  - Yin, Shichang 
                AU  - Wang, Ting 
                AU  - Wang, Yan 
                AU  - Wang, Meiming 
                AU  - Liu, Yixin 
                AU  - Ying, Qiaohui 
                AU  - Sun, Jinrui 
                AU  - Wei, Fulan 
                AU  - Liu, Dongxu 
                AU  - Wang, Chunling 
                AU  - Ge, Shaohua 
                TI  - Down-regulation of long non-coding RNA MEG3 suppresses osteogenic differentiation of periodontal ligament stem cells (PDLSCs) through miR-27a-3p/IGF1 axis in periodontitis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102105
                DO  - 10.18632/aging.102105
                SP  - 5334
                EP  - 5350
                PY  - 
                AB  - Objective: This study aimed to investigate the roles of long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) in osteogenic differentiation of periodontal ligament stem cells (PDLSCs) in periodontitis.Methods: Differentially expressed lncRNAs and mRNAs between periodontitis periodontal ligament tissues and healthy periodontal ligament tissues were selected out using R project. PDLSCs were identified using flow cytometry. Western blot was employed to detect pathway relative proteins. Besides, targeted relationships between lncRNA and miRNA, as well as miRNA and mRNA were verified by dual luciferase reporter gene assay. Osteogenic differentiation of PDLSCs was assessed by alkaline phosphatase (ALP) staining and Alizarin Red Staining (ARS). Markers for osteoblast (Runx2, Osterix, Osteocalcin, Colla1) were detected using western blot.Results: LncRNA MEG3 and IGF1 were both down-regulated, while miR-27a-3p was up-regulated in periodontitis samples compared with healthy samples. Overexpression of MEG3 promoted osteogenic differentiation by enhancing expression of IGF1 yet suppressing expression of miRNA-27a-3p. Meanwhile, the results of ALP and ARS staining indicated that up-regulation of lncRNA MEG3 or IGF1 promoted osteogenic differentiation in PDLSCs, which could be reversed with up-regulation of miRNA-27a-3p.Conclusion: Down-regulation of MEG3 suppressed osteogenic differentiation of PDLSCs through miR-27a-3p/IGF1 axis in periodontitis.
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Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom

Wen Guo, Qing Yu, Ming Zhang, Fang Li, Yu Liu, Weiwei Jiang, Haitao Jiang, Haijun Li,

https://doi.org/10.18632/aging.102109 pp 5351—5367

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Guo W, Yu Q, Zhang M, Li F, Liu Y, Jiang W, Jiang H, Li H, . Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom. . 11:5351-5367. https://doi.org/10.18632/aging.102109

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                TY  - JOUR
                AU  - Guo, Wen 
                AU  - Yu, Qing 
                AU  - Zhang, Ming 
                AU  - Li, Fang 
                AU  - Liu, Yu 
                AU  - Jiang, Weiwei 
                AU  - Jiang, Haitao 
                AU  - Li, Haijun 
                TI  - Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102109
                DO  - 10.18632/aging.102109
                SP  - 5351
                EP  - 5367
                PY  - 
                AB  - Osteosarcoma is a tumor disease that commonly exists among young populations. Our research explored the role of the LINC00511/microRNA-618/MAEL axis in osteosarcoma.Expression profiles of long non-coding RNAs (lncRNAs) in osteosarcoma (OS) tissues were constructed, and LINC00511 expression levels were verified with qRT-PCR. LncRNA-miRNA and miRNA-mRNA interactions were predicted. Validation was performed using a dual-luciferase reporter assay. Protein expression levels of MAEL were evaluated by Western blot assays. The effects of LINC00511, miR-618 and MAEL on the proliferation, viability, and metastasis of OS cells were detected using colony formation, cell counting kit-8 (CCK-8) and transwell assays, respectively. The apoptosis rates of OS cells were investigated using flow cytometry. The tumor-suppressing effect of LINC00511 silencing was also analyzed using a xenograft model in nude mice.LINC00511 overexpression was observed in OS tissues and cell lines. Knockdown of LINC00511 in nude mice inhibited the tumorigenic ability of OS cells. Transfection-induced overexpression of LINC00511 and MAEL, as well as downregulation, highlighted the features of tumor cells, and LINC00511 overexpression reduced apoptosis in vitro.LINC00511 was confirmed to be beneficial for osteosarcoma development via sponging miR-618 and increasing MAEL expression and may thus be considered a potential target for osteosarcoma therapy.
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Downregulation of microRNA-218 is cardioprotective against cardiac fibrosis and cardiac function impairment in myocardial infarction by binding to MITF

Linfeng Qian, Shaobo Pan, Liping Shi, Yongyi Zhou, Lai Sun, Zhedong Wan, Yufang Ding, Jia Qian,

https://doi.org/10.18632/aging.102112 pp 5368—5388

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Qian L, Pan S, Shi L, Zhou Y, Sun L, Wan Z, Ding Y, Qian J, . Downregulation of microRNA-218 is cardioprotective against cardiac fibrosis and cardiac function impairment in myocardial infarction by binding to MITF. . 11:5368-5388. https://doi.org/10.18632/aging.102112

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                TY  - JOUR
                AU  - Qian, Linfeng 
                AU  - Pan, Shaobo 
                AU  - Shi, Liping 
                AU  - Zhou, Yongyi 
                AU  - Sun, Lai 
                AU  - Wan, Zhedong 
                AU  - Ding, Yufang 
                AU  - Qian, Jia 
                TI  - Downregulation of microRNA-218 is cardioprotective against cardiac fibrosis and cardiac function impairment in myocardial infarction by binding to MITF
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102112
                DO  - 10.18632/aging.102112
                SP  - 5368
                EP  - 5388
                PY  - 
                AB  - Objective: This study is intended to figure out the function of microRNA-218 (miR-218) together with microphthalmia-associated transcription factor (MITF) on the cardiac fibrosis and cardiac function impairment in rat models of myocardial infarction (MI).Results: The rats with MI exhibited cardiac function impairment, cardiac fibrosis, oxidative stress, cardiomyocyte apoptosis, as well as inflammatory injury. Additionally, upregulated miR-218 and downregulated MITF were detected in cardiac tissues of MI rats. MI rats injected with miR-218 inhibitors or overexpressed MITF exhibited elevated MITF expression, improved cardiac function, and diminished pathological damages, infarct size, cardiomyocyte apoptosis, cardiac fibrosis, oxidative stress as well as inflammatory injury in cardiac tissues. Furthermore, downregulated miR-218 and MITF aggravated the conditions than downregulation of miR-218 alone in MI rats.Methods: MI models were performed in rats, and then the rats were injected with miR-218 inhibitors and/or MITF overexpression plasmid to elucidate the role of miR-218 and/or MITF on the cardiac function, pathological damage, cardiac fibrosis, angiogenesis, oxidative stress and inflammatory injury of cardiac tissues in MI rats by performing a series of assays.Conclusion: Collectively, we found that the suppression of miR-218 alleviates cardiac fibrosis and cardiac function impairment, and stimulates angiogenesis in MI rats through inhibiting MITF.
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Abnormalities of saccadic eye movements in dementia due to Alzheimer’s disease and mild cognitive impairment

Thomas D.W. Wilcockson, Diako Mardanbegi, Baiqiang Xia, Simon Taylor, Pete Sawyer, Hans W. Gellersen, Ira Leroi, Rebecca Killick, Trevor J. Crawford,

https://doi.org/10.18632/aging.102118 pp 5389—5398

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Wilcockson TD, Mardanbegi D, Xia B, Taylor S, Sawyer P, Gellersen HW, Leroi I, Killick R, Crawford TJ, . Abnormalities of saccadic eye movements in dementia due to Alzheimer’s disease and mild cognitive impairment. . 11:5389-5398. https://doi.org/10.18632/aging.102118

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                TY  - JOUR
                AU  - Wilcockson, Thomas D.W. 
                AU  - Mardanbegi, Diako 
                AU  - Xia, Baiqiang 
                AU  - Taylor, Simon 
                AU  - Sawyer, Pete 
                AU  - Gellersen, Hans W. 
                AU  - Leroi, Ira 
                AU  - Killick, Rebecca 
                AU  - Crawford, Trevor J. 
                TI  - Abnormalities of saccadic eye movements in dementia due to Alzheimer’s disease and mild cognitive impairment
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102118
                DO  - 10.18632/aging.102118
                SP  - 5389
                EP  - 5398
                PY  - 
                AB  - Background: There is increasing evidence that people in the early stages of Alzheimer&#x2019;s disease (AD) have subtle impairments in cognitive inhibition that can be detected by using relatively simple eye-tracking paradigms, but these subtle impairments are often missed by traditional cognitive assessments. People with mild cognitive impairment (MCI) are at an increased likelihood of dementia due to AD. No study has yet investigated and contrasted the MCI subtypes in relation to eye movement performance. Methods: In this work we explore whether eye-tracking impairments can distinguish between patients with the amnesic and the non-amnesic variants of MCI. Participants were 68 people with dementia due to AD, 42 had a diagnosis of aMCI, and 47 had a diagnosis of naMCI, and 92 age-matched cognitively healthy controls. Results: The findings revealed that eye-tracking can distinguish between the two forms of MCI. Conclusions: The work provides further support for eye-tracking as a useful diagnostic biomarker in the assessment of dementia.
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Age-related changes in human sperm DNA integrity

Aleksandra Rosiak-Gill, Kamil Gill, Joanna Jakubik, Monika Fraczek, Lukasz Patorski, Dariusz Gaczarzewicz, Rafał Kurzawa, Maciej Kurpisz, Malgorzata Piasecka,

https://doi.org/10.18632/aging.102120 pp 5399—5411

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Rosiak-Gill A, Gill K, Jakubik J, Fraczek M, Patorski L, Gaczarzewicz D, Kurzawa R, Kurpisz M, Piasecka M, . Age-related changes in human sperm DNA integrity. . 11:5399-5411. https://doi.org/10.18632/aging.102120

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                TY  - JOUR
                AU  - Rosiak-Gill, Aleksandra 
                AU  - Gill, Kamil 
                AU  - Jakubik, Joanna 
                AU  - Fraczek, Monika 
                AU  - Patorski, Lukasz 
                AU  - Gaczarzewicz, Dariusz 
                AU  - Kurzawa, Rafał 
                AU  - Kurpisz, Maciej 
                AU  - Piasecka, Malgorzata 
                TI  - Age-related changes in human sperm DNA integrity
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102120
                DO  - 10.18632/aging.102120
                SP  - 5399
                EP  - 5411
                PY  - 
                AB  - Abnormal standard semen characteristics and reduced sperm chromatin maturity can appear with increasing male age. However, the influence of paternal age on semen parameters is still controversial. Therefore, this study was designed to estimate the influence of paternal age not only on conventional semen characteristics but also on sperm DNA integrity. This research was carried out on ejaculated sperm cells obtained from men (n = 1124) aged &#x2265;40 y and &lt;40 y. Our data revealed a decreased semen volume and an increased percentage of DFI (sperm DNA fragmentation index) in older men compared to younger men in the entire study cohort, in men with normozoospermia and in men with abnormal semen parameters. Moreover, there was a higher incidence of sperm DNA damage (&gt;10% DFI, low fertility potential) in the groups of men aged &#x2265;40 y than in the groups of men aged &lt;40 y. Older men had over twice the odds ratio for high sperm DNA damage as younger men. Our findings suggest a detrimental effect of advanced paternal age on sperm chromatin integrity. The data show that the evaluation of sperm DNA has greater clinical utility than standard semen analysis in case of male fertility potential assessment.
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Sex differences in the associations of placental epigenetic aging with fetal growth

Fasil Tekola-Ayele, Tsegaselassie Workalemahu, Gezahegn Gorfu, Deepika Shrestha, Benjamin Tycko, Ronald Wapner, Cuilin Zhang, Germaine M. Buck Louis,

https://doi.org/10.18632/aging.102124 pp 5412—5432

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Tekola-Ayele F, Workalemahu T, Gorfu G, Shrestha D, Tycko B, Wapner R, Zhang C, Louis GMB, . Sex differences in the associations of placental epigenetic aging with fetal growth. . 11:5412-5432. https://doi.org/10.18632/aging.102124

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                TY  - JOUR
                AU  - Tekola-Ayele, Fasil 
                AU  - Workalemahu, Tsegaselassie 
                AU  - Gorfu, Gezahegn 
                AU  - Shrestha, Deepika 
                AU  - Tycko, Benjamin 
                AU  - Wapner, Ronald 
                AU  - Zhang, Cuilin 
                AU  - Louis, Germaine M. Buck 
                TI  - Sex differences in the associations of placental epigenetic aging with fetal growth
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102124
                DO  - 10.18632/aging.102124
                SP  - 5412
                EP  - 5432
                PY  - 
                AB  - Identifying factors that influence fetal growth in a sex-specific manner can help unravel mechanisms that explain sex differences in adverse neonatal outcomes and in-utero origins of cardiovascular disease disparities. Premature aging of the placenta, a tissue that supports fetal growth and exhibits sex-specific epigenetic changes, is associated with pregnancy complications. Using DNA methylation-based age estimator, we investigated the sex-specific relationship of placental epigenetic aging with fetal growth across 13-40 weeks gestation, neonatal size, and risk of low birth weight. Placental epigenetic age acceleration (PAA), the difference between DNA methylation age and gestational age, was associated with reduced fetal weight among males but with increased fetal weight among females. PAA was inversely associated with fetal weight, abdominal circumference, and biparietal diameter at 32-40 weeks among males but was positively associated with all growth measures among females across 13-40 weeks. A 1-week increase in PAA was associated with 2-fold (95% CI 1.2, 3.2) increased odds for low birth weight and 1.5-fold (95% CI 1.1, 2.0) increased odds for small-for-gestational age among males. In all, fetal growth was significantly reduced in males but not females exposed to a rapidly aging placenta. Epigenetic aging of the placenta may underlie sex differences in neonatal outcomes.
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Genome-wide association study identifies CBFA2T3 affecting the rate of CSF Aβ₄₂ decline in non-demented elders

Kai-Xin Dou, Can Zhang, Chen-Chen Tan, Wei Xu, Jie-Qiong Li, Xi-Peng Cao, Lan Tan, Jin-Tai Yu, for the Alzheimer’s Disease Neuroimaging Initiative (ADNI),

https://doi.org/10.18632/aging.102125 pp 5433—5444

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Dou K, Zhang C, Tan C, Xu W, Li J, Cao X, Tan L, Yu J, , . Genome-wide association study identifies CBFA2T3 affecting the rate of CSF Aβ₄₂ decline in non-demented elders. . 11:5433-5444. https://doi.org/10.18632/aging.102125

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Provider: 
 TY - JOUR
 AU - Dou, Kai-Xin 
 AU - Zhang, Can 
 AU - Tan, Chen-Chen 
 AU - Xu, Wei 
 AU - Li, Jie-Qiong 
 AU - Cao, Xi-Peng 
 AU - Tan, Lan 
 AU - Yu, Jin-Tai 
 AU - , 
 TI - Genome-wide association study identifies CBFA2T3 affecting the rate of CSF Aβ42 decline in non-demented elders
 JO - 
 JA - 
 VL - 11
 IS - 15
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102125
 DO - 10.18632/aging.102125
 SP - 5433
 EP - 5444
 PY - 
 AB - Brain amyloid deposition is an early pathological event in Alzheimer&#x2019;s disease (AD), and abnormally low levels amyloid-&#x3B2;42 peptide (A&#x3B2;42) in cerebrospinal fluid (CSF) can be detected in preclinical AD. To identify the genetic determinants that regulate the rate of CSF A&#x3B2;42 decline among non-demented elders, we conducted a genome-wide association study involved 321 non-demented elders from Alzheimer&#x2019;s Disease Neuroimaging Initiative (ADNI) 1/GO/2 cohorts restricted to non-Hispanic Caucasians. A novel genome-wide significant association of higher annualized percent decline of CSF A&#x3B2;42 in the gene CBFA2T3 (CBFA2/RUNX1 translocation partner 3; rs13333659-T; p = 2.24 &#xD7; 10&#x2212;9) was identified. Besides displaying abnormal CSF A&#x3B2;42 levels, rs13333659-T carriers were more likely to exhibit a greater longitudinal cognitive decline (p = 0.029, &#x3B2; = 0.097) and hippocampal atrophy (p = 0.029, &#x3B2; = &#x2212;0.160) in the non-demented elders, especially for the participants who were amyloid-positive at baseline. These findings suggest rs13333659 in CBFA2T3 as a risk locus to modulate the decline rate of CSF A&#x3B2;42 preceding the onset of clinical symptoms.
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Impact of C-reactive protein on osteo-/chondrogenic transdifferentiation and calcification of vascular smooth muscle cells

Laura A. Henze, Trang T.D. Luong, Beate Boehme, Jaber Masyout, Markus P. Schneider, Sebastian Brachs, Florian Lang, Burkert Pieske, Andreas Pasch, Kai-Uwe Eckardt, Jakob Voelkl, Ioana Alesutan,

https://doi.org/10.18632/aging.102130 pp 5445—5462

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Henze LA, Luong TT, Boehme B, Masyout J, Schneider MP, Brachs S, Lang F, Pieske B, Pasch A, Eckardt K, Voelkl J, Alesutan I, . Impact of C-reactive protein on osteo-/chondrogenic transdifferentiation and calcification of vascular smooth muscle cells. . 11:5445-5462. https://doi.org/10.18632/aging.102130

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                TY  - JOUR
                AU  - Henze, Laura A. 
                AU  - Luong, Trang T.D. 
                AU  - Boehme, Beate 
                AU  - Masyout, Jaber 
                AU  - Schneider, Markus P. 
                AU  - Brachs, Sebastian 
                AU  - Lang, Florian 
                AU  - Pieske, Burkert 
                AU  - Pasch, Andreas 
                AU  - Eckardt, Kai-Uwe 
                AU  - Voelkl, Jakob 
                AU  - Alesutan, Ioana 
                TI  - Impact of C-reactive protein on osteo-/chondrogenic transdifferentiation and calcification of vascular smooth muscle cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102130
                DO  - 10.18632/aging.102130
                SP  - 5445
                EP  - 5462
                PY  - 
                AB  - Medial vascular calcification occurs during the aging process and is strongly accelerated by chronic kidney disease (CKD). Elevated C-reactive protein (CRP) levels are associated with vascular calcification, cardiovascular events and mortality in CKD patients. CRP is an important promoter of vascular inflammation. Inflammatory processes are critically involved in initiation and progression of vascular calcification. Thus, the present study explored a possible impact of CRP on vascular calcification. We found that CRP promoted osteo-/chondrogenic transdifferentiation and aggravated phosphate-induced osteo-/chondrogenic transdifferentiation and calcification of primary human aortic smooth muscle cells (HAoSMCs). These effects were paralleled by increased cellular oxidative stress and corresponding pro-calcific downstream-signaling. Antioxidants or p38 MAPK inhibition suppressed CRP-induced osteo-/chondrogenic signaling and mineralization. Furthermore, silencing of Fc fragment of IgG receptor IIa (FCGR2A) blunted the pro-calcific effects of CRP. Vascular CRP expression was increased in the klotho-hypomorphic mouse model of aging as well as in HAoSMCs during calcifying conditions. In conclusion, CRP augments osteo-/chondrogenic transdifferentiation of vascular smooth muscle cells through mechanisms involving FCGR2A-dependent induction of oxidative stress. Thus, systemic inflammation may actively contribute to the progression of vascular calcification.
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Large-scale analysis reveals the specific clinical and immune features of CD155 in glioma

Fangkun Liu, Jing Huang, Yuanyuan Xiong, Shuwang Li, Zhixiong Liu,

https://doi.org/10.18632/aging.102131 pp 5463—5482

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Liu F, Huang J, Xiong Y, Li S, Liu Z, . Large-scale analysis reveals the specific clinical and immune features of CD155 in glioma. . 11:5463-5482. https://doi.org/10.18632/aging.102131

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                TY  - JOUR
                AU  - Liu, Fangkun 
                AU  - Huang, Jing 
                AU  - Xiong, Yuanyuan 
                AU  - Li, Shuwang 
                AU  - Liu, Zhixiong 
                TI  - Large-scale analysis reveals the specific clinical and immune features of CD155 in glioma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102131
                DO  - 10.18632/aging.102131
                SP  - 5463
                EP  - 5482
                PY  - 
                AB  - Recent studies demonstrated that CD155 plays an important role in anti-tumor immune responses. However, its role in glioma remains unclear. Here, we identify CD155 as a promising immune target in glioma. CD155 expression was significantly highly expressed in glioblastoma but not in normal brain tissue. Subsequent analysis based on genetic and clinical data from 1173 glioma patients in Rembrandt and TCGA dataset suggested that CD155 related genes of immune response were mainly positively correlated with CD155 expression. CD155 expression was positively correlated with immune-related metagenes STAT1, HCK, LCK, and MHC I but negatively associated with IgG. CD155 expression was positively correlated with biomarker gene expression of infiltrating immune cells, suggested that high CD155 expression in gliomas tend to have more infiltrating immune cells compared with gliomas with low CD155 expression. Pearson correlation analysis showed that CD155 is associated with CD96, CD226, Nectin4, PD-L1, B7-H2, NR2F6 and GITR, implying the potential synergistic effects of these checkpoint proteins. These findings implied that CD155 is a promising immunotherapy target, combined with existing immune checkpoint blockade therapies for glioma.
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CBX3/HP1γ promotes tumor proliferation and predicts poor survival in hepatocellular carcinoma

Xiaoping Zhong, Anna Kan, Wancong Zhang, Jianda Zhou, Huayong Zhang, Jiasheng Chen, Shijie Tang,

https://doi.org/10.18632/aging.102132 pp 5483—5497

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Zhong X, Kan A, Zhang W, Zhou J, Zhang H, Chen J, Tang S, . CBX3/HP1γ promotes tumor proliferation and predicts poor survival in hepatocellular carcinoma. . 11:5483-5497. https://doi.org/10.18632/aging.102132

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                TY  - JOUR
                AU  - Zhong, Xiaoping 
                AU  - Kan, Anna 
                AU  - Zhang, Wancong 
                AU  - Zhou, Jianda 
                AU  - Zhang, Huayong 
                AU  - Chen, Jiasheng 
                AU  - Tang, Shijie 
                TI  - CBX3/HP1γ promotes tumor proliferation and predicts poor survival in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102132
                DO  - 10.18632/aging.102132
                SP  - 5483
                EP  - 5497
                PY  - 
                AB  - HP1&#x3B3;, encoded by CBX3, is associated with cancer progression and patient prognosis. However, the prognostic value and functions of CBX3/HP1&#x3B3; in hepatocellular carcinoma (HCC) remain unclear. Here, we performed a bioinformatics analysis using the Oncomine, TCGA and Human Protein Atlas databases, the Kaplan-Meier plotter, and the UALCAN web-portal to explore the expression and prognostic significance of CBX3/HP1&#x3B3; in patients with different cancers, including liver cancer. HCC tissues and microarrays containing 354 samples were examined using immunohistochemical staining, quantitative real-time polymerase chain reaction, and Western blotting. CBX3-overexpression HCC cell lines were tested in proliferation assays to determine the function of CBX3/HP1&#x3B3;. We found that CBX3/HP1&#x3B3; was upregulated in many cancers and was associated with poor prognosis. Our results also revealed that CBX3/HP1&#x3B3; is elevated in HCC tissues and is associated with malignant clinicopathological characteristics. Kaplan-Meier and Cox regression analyses verified that high CBX3/HP1&#x3B3; expression is an independent and significant prognostic factor for reduced overall survival in HCC patients. Moreover, in vitro functional assays showed that CBX3/HP1&#x3B3; overexpression promotes HCC cell proliferation. These findings suggest that CBX3/HP1&#x3B3; is an important oncogene in HCC that might act as a useful biomarker for prognosis and targeted therapy.
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Environmental exposure to polybrominated biphenyl (PBB) associates with an increased rate of biological aging

Sarah W. Curtis, Dawayland O. Cobb, Varun Kilaru, Metrecia L. Terrell, M. Elizabeth Marder, Dana Boyd Barr, Carmen J. Marsit, Michele Marcus, Karen N. Conneely, Alicia K. Smith,

https://doi.org/10.18632/aging.102134 pp 5498—5517

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Curtis SW, Cobb DO, Kilaru V, Terrell ML, Marder ME, Barr DB, Marsit CJ, Marcus M, Conneely KN, Smith AK, . Environmental exposure to polybrominated biphenyl (PBB) associates with an increased rate of biological aging. . 11:5498-5517. https://doi.org/10.18632/aging.102134

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                TY  - JOUR
                AU  - Curtis, Sarah W. 
                AU  - Cobb, Dawayland O. 
                AU  - Kilaru, Varun 
                AU  - Terrell, Metrecia L. 
                AU  - Marder, M. Elizabeth 
                AU  - Barr, Dana Boyd 
                AU  - Marsit, Carmen J. 
                AU  - Marcus, Michele 
                AU  - Conneely, Karen N. 
                AU  - Smith, Alicia K. 
                TI  - Environmental exposure to polybrominated biphenyl (PBB) associates with an increased rate of biological aging
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102134
                DO  - 10.18632/aging.102134
                SP  - 5498
                EP  - 5517
                PY  - 
                AB  - Advanced age increases risk for cancer, cardiovascular disease, and all-cause mortality. However, people do not age at the same rate, and biological age (frequently measured through DNA methylation) can be older than chronological age. Environmental factors have been associated with the rate of biological aging, but it is not known whether persistent endocrine-disrupting compounds (EDCs) like polybrominated biphenyl (PBB) would associate with age acceleration. Three different epigenetic age acceleration measures (intrinsic, extrinsic, and phenotypic) were calculated from existing epigenetic data in whole blood from a population highly exposed to PBB (N=658). Association between serum PBB concentration and these measures was tested, controlling for sex, lipid levels, and estimated cell type proportions. Higher PBB levels associated with increased age acceleration (intrinsic: &#x3B2;=0.24, 95%CI=0.01-0.46, p = 0.03; extrinsic: &#x3B2;=0.39, 95%CI=0.12-0.65, p = 0.004; and phenotypic: &#x3B2;=0.30, 95%CI=0.05-0.54, p = 0.01). Neither age when exposed to PBB nor sex statistically interacted with PBB to predict age acceleration, but, in stratified analyses, the association between PBB and age acceleration was only in people exposed before finishing puberty and in men. This suggests that EDCs can associate with the biological aging process, and further studies are warranted to investigate other environmental pollutants&#x2019; effect on aging.
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Frailty in middle age is associated with frailty status and race-specific changes to the transcriptome

Calais S. Prince, Nicole Noren Hooten, Nicolle A. Mode, Yongqing Zhang, Ngozi Ejiogu, Kevin G. Becker, Alan B. Zonderman, Michele K. Evans,

https://doi.org/10.18632/aging.102135 pp 5518—5534

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Prince CS, Noren Hooten N, Mode NA, Zhang Y, Ejiogu N, Becker KG, Zonderman AB, Evans MK, . Frailty in middle age is associated with frailty status and race-specific changes to the transcriptome. . 11:5518-5534. https://doi.org/10.18632/aging.102135

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                TY  - JOUR
                AU  - Prince, Calais S. 
                AU  - Noren Hooten, Nicole 
                AU  - Mode, Nicolle A. 
                AU  - Zhang, Yongqing 
                AU  - Ejiogu, Ngozi 
                AU  - Becker, Kevin G. 
                AU  - Zonderman, Alan B. 
                AU  - Evans, Michele K. 
                TI  - Frailty in middle age is associated with frailty status and race-specific changes to the transcriptome
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102135
                DO  - 10.18632/aging.102135
                SP  - 5518
                EP  - 5534
                PY  - 
                AB  - Frailty is an aging-associated syndrome resulting from diminished capacity to respond to stressors and is a significant risk factor for disability and mortality. Although frailty is usually studied in old age, it is present in mid-life. Given the increases in mortality statistics among middle-aged Americans, understanding molecular drivers of frailty in a younger, diverse cohort may facilitate identifying pathways for early intervention. We analyzed frailty-associated, genome-wide transcriptional changes in middle-aged blacks and whites. Next generation RNA sequencing was completed using total RNA from peripheral blood mononuclear cells (n = 16). We analyzed differential gene expression patterns and completed a parametric analysis of gene set enrichment (PAGE). Differential gene expression was validated using RT-qPCR (n = 52). We identified 5,082 genes differentially expressed with frailty. Frailty altered gene expression patterns and biological pathways differently in blacks and whites, including pathways related to inflammation and immunity. The validation study showed a significant two-way interaction between frailty, race, and expression of the cytokine IL1B and the transcription factor EGR1. The glucose transporter, SLC2A6, the neutrophil receptor, FCGR3B, and the accessory protein, C17orf56, were decreased with frailty. These results suggest that there may be demographic dependent, divergent biological pathways underlying frailty in middle-aged adults.
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HO-1 reduces heat stress-induced apoptosis in bovine granulosa cells by suppressing oxidative stress

Yiru Wang, Caixia Yang, Nahla Abdalla Hassan Elsheikh, Chengmin Li, Fangxiao Yang, Genlin Wang, Lian Li,

https://doi.org/10.18632/aging.102136 pp 5535—5547

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Wang Y, Yang C, Elsheikh NA, Li C, Yang F, Wang G, Li L, . HO-1 reduces heat stress-induced apoptosis in bovine granulosa cells by suppressing oxidative stress. . 11:5535-5547. https://doi.org/10.18632/aging.102136

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                TY  - JOUR
                AU  - Wang, Yiru 
                AU  - Yang, Caixia 
                AU  - Elsheikh, Nahla Abdalla Hassan
                AU  - Li, Chengmin 
                AU  - Yang, Fangxiao 
                AU  - Wang, Genlin 
                AU  - Li, Lian 
                TI  - HO-1 reduces heat stress-induced apoptosis in bovine granulosa cells by suppressing oxidative stress
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102136
                DO  - 10.18632/aging.102136
                SP  - 5535
                EP  - 5547
                PY  - 
                AB  - Heat stress negatively affects reproduction in cattle by disrupting the normal function of ovarian granulosa cells (GCs), ultimately leading to oxidative damage and cell death via apoptosis. Heme oxygenase-1(HO-1) is a member of the heat shock protein family, which are associated with cellular antioxidant defenses and anti-apoptotic functions. Recent studies demonstrated that HO-1 is upregulated in heat-stressed cells. In the present study, we investigated the expression of HO-1 in bovine GCs transiently exposed to heat stress and characterized the expression and activity of key oxidative stress enzymes and molecules. We show that heat stress induced oxidative stress and apoptosis, and enhanced Nrf2 and HO-1 expression in primary GC cultures. Knocking down HO-1 expression using siRNA exacerbated both oxidative stress and apoptosis, whereas pre-treating GCs with hemin, which induces HO-1 expression, partially prevented these effects. These findings demonstrate that HO-1 attenuates heat stress-induced apoptosis in bovine GCs by decreasing production of reactive oxygen species and activating the antioxidant response.
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Ginseng increases Klotho expression by FoxO3-mediated manganese superoxide dismutase in a mouse model of tacrolimus-induced renal injury

Sun Woo Lim, Yoo Jin Shin, Kang Luo, Yi Quan, Sheng Cui, Eun Jeong Ko, Byung Ha Chung, Chul Woo Yang,

https://doi.org/10.18632/aging.102137 pp 5548—5569

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Lim SW, Shin YJ, Luo K, Quan Y, Cui S, Ko EJ, Chung BH, Yang CW, . Ginseng increases Klotho expression by FoxO3-mediated manganese superoxide dismutase in a mouse model of tacrolimus-induced renal injury. . 11:5548-5569. https://doi.org/10.18632/aging.102137

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                TY  - JOUR
                AU  - Lim, Sun Woo 
                AU  - Shin, Yoo Jin 
                AU  - Luo, Kang 
                AU  - Quan, Yi 
                AU  - Cui, Sheng 
                AU  - Ko, Eun Jeong 
                AU  - Chung, Byung Ha 
                AU  - Yang, Chul Woo 
                TI  - Ginseng increases Klotho expression by FoxO3-mediated manganese superoxide dismutase in a mouse model of tacrolimus-induced renal injury
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102137
                DO  - 10.18632/aging.102137
                SP  - 5548
                EP  - 5569
                PY  - 
                AB  - The antioxidant function of Klotho is well-documented as a regulatory factor implicated in countering the aging process. This study investigated whether ginseng upregulates Klotho and its antiaging signaling in a setting of calcineurin inhibitor-induced oxidative stress. Although tacrolimus treatment reduced Klotho level in the serum and kidney, ginseng treatment was found to reverse the levels. Tacrolimus-induced oxidative stress was reduced by ginseng treatment, with functional and histological improvements. Effect of ginseng on Klotho-induced manganese superoxide dismutase signaling pathway during tacrolimus treatment in mice revealed that ginseng suppressed phosphatidylinositol 3-kinase/serine-threonine kinase Akt-mediated phosphorylation of forkhead box protein O3a and promoted the binding of forkhead box protein O3a to manganese superoxide dismutase promoter. In the mitochondria, ginseng reduced mitochondrial reactive oxygen species production, mitochondrial membrane potential, and oxygen consumption rate, whereas blocking phosphatidylinositol 3-kinase activity with LY294002 enhanced them. These findings together suggested that ginseng attenuated tacrolimus-induced oxidative stress via signaling between Klotho and the phosphatidylinositol 3-kinase/serine-threonine kinase Akt/forkhead box protein O3a-related antioxidant pathway.
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Effects of inflammatory responses, apoptosis, and STAT3/NF-κB- and Nrf2-mediated oxidative stress on benign prostatic hyperplasia induced by a high-fat diet

Yongzhi Li, Benkang Shi, Fengming Dong, Xingwang Zhu, Bing Liu, Yili Liu,

https://doi.org/10.18632/aging.102138 pp 5570—5578

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Li Y, Shi B, Dong F, Zhu X, Liu B, Liu Y, . Effects of inflammatory responses, apoptosis, and STAT3/NF-κB- and Nrf2-mediated oxidative stress on benign prostatic hyperplasia induced by a high-fat diet. . 11:5570-5578. https://doi.org/10.18632/aging.102138

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                TY  - JOUR
                AU  - Li, Yongzhi 
                AU  - Shi, Benkang 
                AU  - Dong, Fengming 
                AU  - Zhu, Xingwang 
                AU  - Liu, Bing 
                AU  - Liu, Yili 
                TI  - Effects of inflammatory responses, apoptosis, and STAT3/NF-κB- and Nrf2-mediated oxidative stress on benign prostatic hyperplasia induced by a high-fat diet
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102138
                DO  - 10.18632/aging.102138
                SP  - 5570
                EP  - 5578
                PY  - 
                AB  - This study determined whether or not benign prostatic hyperplasia (BPH) induced by a high-fat diet (HFD) is involved in inflammatory responses, apoptosis, and the signal transducer and activator of transcription (STAT3)/nuclear factor-kappa B (NF-&#x3BA;B)- and nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated oxidative stress pathways. Forty rats were divided into four groups: control; HFD; testosterone; and HFD+testosterone. Hematoxylin and eosin (HE) staining was used to assess histologic changes. An enzyme-linked immunosorbent assay and Western blot analysis were used to detect levels of related proteins. Compared with the control group, the prostate levels of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-&#x3B1; (TNF-&#x3B1;), interleukin-6 (IL-6), malondialdehyde (MDA), transforming growth factor-&#x3B2;1 (TGF-&#x3B2;1), and monocyte chemotactic protein-1 (MCP-1) were significantly increased, while the levels of glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione (GSH), and superoxide dismutase (SOD) were decreased. The TNF-&#x3BA;B, Bcl-2, and caspase-3 levels were increased, while the Bax level was markedly decreased. The cytoplasmic expression of STAT3 and NF-&#x3BA;B was increased, while the nuclear expression of Nrf2 was markedly decreased compared with the control group. In summary, our results demonstrated that a long-term HFD might cause changes in inflammatory responses, apoptosis, and oxidative stress, thus contributing to prostatic hyperplasia. The underlying mechanisms might be related to the STAT3/NF-&#x3BA;B- and Nrf2-mediated oxidative stress pathway.
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Integrative analysis of DNA methylation and gene expression to identify key epigenetic genes in glioblastoma

Danyun Jia, Wei Lin, Hongli Tang, Yifan Cheng, Kaiwei Xu, Yanshu He, Wujun Geng, Qinxue Dai,

https://doi.org/10.18632/aging.102139 pp 5579—5592

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Jia D, Lin W, Tang H, Cheng Y, Xu K, He Y, Geng W, Dai Q, . Integrative analysis of DNA methylation and gene expression to identify key epigenetic genes in glioblastoma. . 11:5579-5592. https://doi.org/10.18632/aging.102139

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                TY  - JOUR
                AU  - Jia, Danyun 
                AU  - Lin, Wei 
                AU  - Tang, Hongli 
                AU  - Cheng, Yifan 
                AU  - Xu, Kaiwei 
                AU  - He, Yanshu 
                AU  - Geng, Wujun 
                AU  - Dai, Qinxue 
                TI  - Integrative analysis of DNA methylation and gene expression to identify key epigenetic genes in glioblastoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102139
                DO  - 10.18632/aging.102139
                SP  - 5579
                EP  - 5592
                PY  - 
                AB  - Glioblastoma (GBM) ranks the most common and aggressive primary brain malignant tumor worldwide. However, the survival rates of patients remain very poor. Therefore, molecular oncology of GBM are urgently needed. In this study, we performed an integrative analysis of DNA methylation and gene expression to identify key epigenetic genes in GBM. The methylation and gene expression of GBM patients in The Cancer Genome Atlas (TCGA) database were downloaded. After data preprocessing, we identified 4,881 differentially expressed genes (DEGs) between tumor and normal samples, including 1,111 upregulated and 3,770 downregulated genes. Then, we randomly separated all samples into training set (n = 69) and testing set (n = 69). We next obtained 11,269 survival-methylation sites by univariate and multivariate Cox regression analyses. In the correlation analysis, we defined 198 low promoter methylation with high gene expression as epigenetically induced (EI) genes and 111 high promoter methylation with low gene expression as epigenetically suppressed (ES) genes. Key markers including C1orf61 and FAM50B were selected with a Pearson correlation coefficient greater than 0.75. Further, we chose the 20 CpG methylation sites of above two genes in unsupervised clustering analysis using the Euclidean distance. We found that the prognosis of the hypomethylated group was significantly better than that in the hypermethylated group (log-rank test p-value = 0.011). Based on the validation in the TCGA testing set and GEO dataset, we validated the prognostic value of our signature (p-value = 0.02 in TCGA and 0.012 in GEO). In conclusion, our findings provided predictive and prognostic value as methylation-based biomarkers for the diagnosis and treatment of GBM.
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TGFβ1- miR-140-5p axis mediated up-regulation of Flap Endonuclease 1 promotes epithelial-mesenchymal transition in hepatocellular carcinoma

Chuanfei Li, Di Zhou, Hao Hong, Shuangyan Yang, Li Zhang, Shiying Li, Peng Hu, Hong Ren, Zhechuan Mei, Hui Tang,

https://doi.org/10.18632/aging.102140 pp 5593—5612

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Li C, Zhou D, Hong H, Yang S, Zhang L, Li S, Hu P, Ren H, Mei Z, Tang H, . TGFβ1- miR-140-5p axis mediated up-regulation of Flap Endonuclease 1 promotes epithelial-mesenchymal transition in hepatocellular carcinoma. . 11:5593-5612. https://doi.org/10.18632/aging.102140

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                TY  - JOUR
                AU  - Li, Chuanfei 
                AU  - Zhou, Di 
                AU  - Hong, Hao 
                AU  - Yang, Shuangyan 
                AU  - Zhang, Li 
                AU  - Li, Shiying 
                AU  - Hu, Peng 
                AU  - Ren, Hong 
                AU  - Mei, Zhechuan 
                AU  - Tang, Hui 
                TI  - TGFβ1- miR-140-5p axis mediated up-regulation of Flap Endonuclease 1 promotes epithelial-mesenchymal transition in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102140
                DO  - 10.18632/aging.102140
                SP  - 5593
                EP  - 5612
                PY  - 
                AB  - Flap Endonuclease 1 (FEN1) is a known oncogene in an array of cancers, but its role in hepatocellular carcinoma (HCC) remains obscure. In this study, we report that FEN1 expression was elevated in the Cancer Genome Atlas (TCGA) database which was verified in HCC tissue and hepatoma cell lines. Pearson correlation analysis indicated that FEN1 was involved in HCC metastasis. We demonstrated that FEN1 silencing inhibits HCC cell epithelial-mesenchymal transition (EMT), invasion and migration in vitro and significantly suppressed tumor growth and metastasis in vivo. Conversely, FEN1 overexpression in HCC cells enhanced these metastatic processes. We further confirmed that FEN1 was a direct target of miR-140-5p, which was down-regulated in HCC tissues, and negatively correlated with FEN1 expression. Moreover, low miR-140-5p levels and high FEN1 expression predicted a poor clinical outcome. The effects of FEN1 overexpression could be partially abolished by miR-140-5p. miR-140-5p down-regulation and FEN1 overexpression were observed in a TGF&#x3B2;1 induced EMT model. TGF&#x3B2;1 mediated EMT could be blocked by miR-140-5p overexpression or FEN1 silencing. Taken together, our findings suggest that FEN1 is regulated by the TGF&#x3B2;1- miR-140-5p axis and promotes EMT in HCC.
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Androgen deprivation therapy increases brain ageing

Julio Plata-Bello, Ana Plata-Bello, Yaiza Pérez-Martín, Victor Fajardo, Tomás Concepción-Massip,

https://doi.org/10.18632/aging.102142 pp 5613—5627

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Plata-Bello J, Plata-Bello A, Pérez-Martín Y, Fajardo V, Concepción-Massip T, . Androgen deprivation therapy increases brain ageing. . 11:5613-5627. https://doi.org/10.18632/aging.102142

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                TY  - JOUR
                AU  - Plata-Bello, Julio 
                AU  - Plata-Bello, Ana 
                AU  - Pérez-Martín, Yaiza 
                AU  - Fajardo, Victor 
                AU  - Concepción-Massip, Tomás 
                TI  - Androgen deprivation therapy increases brain ageing
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102142
                DO  - 10.18632/aging.102142
                SP  - 5613
                EP  - 5627
                PY  - 
                AB  - Background: Prostate cancer (PC) is the most frequent neoplasia in the male population and androgen deprivation therapy (ADT) is frequently used in the management of the disease.Aim: To evaluate the effect of ADT exposure on cognitive status, grey matter volume (GMV) and white matter lesion (WML) load.Methods: Fifty ADT patients and fifteen PC-non-ADT (control) patients were included in the study. A neuropsychological evaluation was performed and a magnetic resonance imaging (MRI), with anatomical T1 and FLAIR sequences, was performed to evaluate the GMV and the WML burden.Results: Most of the patients included in the study presented a significant cognitive impairment (CI). No significant differences were identified in the cognitive assessment between the studied groups, but when considering the educational background intragroup differences were found.No significant difference of GMV and WML volume were identified between groups, but a negative relationship between the ADT period and the GMV was identified. Furthermore, a significant positive association between the age and the lesion volume was found in the ADT group (&#x3B2;=.406; p=.004).Conclusion: PC patients exposed to ADT present an acceleration of age-related brain changes, such as WML development and GMV loss.
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Rejuvenation of brain, liver and muscle by simultaneous pharmacological modulation of two signaling determinants, that change in opposite directions with age

Melod Mehdipour, Jessy Etienne, Chia-Chien Chen, Ranveer Gathwala, Maryam Rehman, Cameron Kato, Chao Liu, Yutong Liu, Yi Zuo, Michael J. Conboy, Irina M. Conboy,

https://doi.org/10.18632/aging.102148 pp 5628—5645

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Mehdipour M, Etienne J, Chen C, Gathwala R, Rehman M, Kato C, Liu C, Liu Y, Zuo Y, Conboy MJ, Conboy IM, . Rejuvenation of brain, liver and muscle by simultaneous pharmacological modulation of two signaling determinants, that change in opposite directions with age. . 11:5628-5645. https://doi.org/10.18632/aging.102148

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                TY  - JOUR
                AU  - Mehdipour, Melod 
                AU  - Etienne, Jessy 
                AU  - Chen, Chia-Chien 
                AU  - Gathwala, Ranveer 
                AU  - Rehman, Maryam 
                AU  - Kato, Cameron 
                AU  - Liu, Chao 
                AU  - Liu, Yutong 
                AU  - Zuo, Yi 
                AU  - Conboy, Michael J. 
                AU  - Conboy, Irina M. 
                TI  - Rejuvenation of brain, liver and muscle by simultaneous pharmacological modulation of two signaling determinants, that change in opposite directions with age
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102148
                DO  - 10.18632/aging.102148
                SP  - 5628
                EP  - 5645
                PY  - 
                AB  - We hypothesize that altered intensities of a few morphogenic pathways account for most/all the phenotypes of aging. Investigating this has revealed a novel approach to rejuvenate multiple mammalian tissues by defined pharmacology. Specifically, we pursued the simultaneous youthful in vivo calibration of two determinants: TGF-beta which activates ALK5/pSmad 2,3 and goes up with age, and oxytocin (OT) which activates MAPK and diminishes with age. The dose of Alk5 inhibitor (Alk5i) was reduced by 10-fold and the duration of treatment was shortened (to minimize overt skewing of cell-signaling pathways), yet the positive outcomes were broadened, as compared with our previous studies. Alk5i plus OT quickly and robustly enhanced neurogenesis, reduced neuro-inflammation, improved cognitive performance, and rejuvenated livers and muscle in old mice. Interestingly, the combination also diminished the numbers of cells that express the CDK inhibitor and marker of senescence p16 in vivo. Summarily, simultaneously re-normalizing two pathways that change with age in opposite ways (up vs. down) synergistically reverses multiple symptoms of aging.
                ER  -

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The long noncoding RNA MIR210HG promotes tumor metastasis by acting as a ceRNA of miR-1226-3p to regulate mucin-1c expression in invasive breast cancer

Xiao-yu Li, Li-ye Zhou, Hao Luo, Qi Zhu, Liang Zuo, Gu-yue Liu, Chu Feng, Jun-yong Zhao, Yuan-yuan Zhang, Xue Li,

https://doi.org/10.18632/aging.102149 pp 5646—5665

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Li X, Zhou L, Luo H, Zhu Q, Zuo L, Liu G, Feng C, Zhao J, Zhang Y, Li X, . The long noncoding RNA MIR210HG promotes tumor metastasis by acting as a ceRNA of miR-1226-3p to regulate mucin-1c expression in invasive breast cancer. . 11:5646-5665. https://doi.org/10.18632/aging.102149

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                TY  - JOUR
                AU  - Li, Xiao-yu 
                AU  - Zhou, Li-ye 
                AU  - Luo, Hao 
                AU  - Zhu, Qi 
                AU  - Zuo, Liang 
                AU  - Liu, Gu-yue 
                AU  - Feng, Chu 
                AU  - Zhao, Jun-yong 
                AU  - Zhang, Yuan-yuan 
                AU  - Li, Xue 
                TI  - The long noncoding RNA MIR210HG promotes tumor metastasis by acting as a ceRNA of miR-1226-3p to regulate mucin-1c expression in invasive breast cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102149
                DO  - 10.18632/aging.102149
                SP  - 5646
                EP  - 5665
                PY  - 
                AB  - Background: Long noncoding RNAs have been known to be involved in multiple types of malignancies, including invasive breast cancer (IBC). This study aimed to explore the role of long noncoding RNAs in IBC and elucidate the potential molecular mechanisms.Methods: Using TCGA microarray data analysis, we identified a long noncoding RNA, MIR210HG, highly expressed in IBC. Kaplan-Meier method and the log-rank test were used for survival analysis. The gain-of-function experiments were performed to assess the function of MIR210HG in IBC invasion and migration in both in vitro and in vivo settings. Bioinformatic analysis as well as luciferase reporter assay, rescue experiments and western blot assay revealed the mode of action of MIR210HG.Results: The aberrantly enhanced MiR210HG expression predicted poor prognosis and lower survival rate. Knockdown of MiR210HG suppressed IBC cell invasion and metastasis both in vitro and in vivo. MiR-1226-3p was identified and validated to be the target miRNA of MiR210HG. Furthermore, MiR210HG functions as a competing endogenous RNAs (ceRNA) which sponges miR-1226-3p, therefore upregulates the expression of mucin1 (MUC1-C).Conclusions: Our study demonstrated that MiR210HG sponges miR-1226-3p to facilitate invasive breast cancer cell invasion and metastasis by regulating mucin-1c and EMT pathway, revealing the oncogenic role of MiR210HG in IBC cells.
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Overexpressed pseudogenes, DUXAP8 and DUXAP9, promote growth of renal cell carcinoma and serve as unfavorable prognostic biomarkers

Jing Chen, Weiyang Lou, Bisha Ding, Xian Wang,

https://doi.org/10.18632/aging.102152 pp 5666—5688

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Chen J, Lou W, Ding B, Wang X, . Overexpressed pseudogenes, DUXAP8 and DUXAP9, promote growth of renal cell carcinoma and serve as unfavorable prognostic biomarkers. . 11:5666-5688. https://doi.org/10.18632/aging.102152

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                TY  - JOUR
                AU  - Chen, Jing 
                AU  - Lou, Weiyang 
                AU  - Ding, Bisha 
                AU  - Wang, Xian 
                TI  - Overexpressed pseudogenes, DUXAP8 and DUXAP9, promote growth of renal cell carcinoma and serve as unfavorable prognostic biomarkers
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102152
                DO  - 10.18632/aging.102152
                SP  - 5666
                EP  - 5688
                PY  - 
                AB  - Background: Growing studies have reported that pseudogenes play key roles in multiple human cancers. However, expression and roles of pseudogenes in renal cell carcinoma remains absent.Results: 31 upregulated and 16 downregulated pseudogenes were screened. Higher expression of DUXAP8 and DUXAP9 indicated poorer prognosis of kidney cancer. 33 and 5 miRNAs were predicted to potentially binding to DUXAP8 and DUXAP9, respectively. miR-29c-3p was identified as the most potential binding miRNAs of DUXAP8 and DUXAP9 based on expression, survival and correlation analyses. 254 target genes of miR-29c-3p were forecast. 47 hub genes with node degree &gt;= 10 were identified. Subsequent analysis for the top 10 hub genes demonstrated that COL1A1 and COL1A2 may be two functional targets of DUXAP8 and DUXAP9. Expression of DUXAP8, DUXAP9, COL1A1 and COL1A2 were significantly increased in cancer samples compared to normal controls while miR-29c-3p expression was decreased. Luciferase reporter assay revealed that miR-29c-3p could directly bind to DUXAP8, DUXAP9, COL1A1 and COL1A2. Functional experiments showed that DUXAP8 and DUXAP9 enhanced but miR-29c-3p weakened growth of renal cell carcinoma.Conclusions: In conclusion, upregulated DUXAP8 and DUXAP9 promote growth of renal cell carcinoma and serve as two promising prognostic biomarkers.Methods: Dysregulated pseudogenes were obtained by dreamBase and GEPIA. The binding miRNAs of pseudogene and targets of miRNA were predicted using starBase and miRNet. Kaplan-Meier plotter was utilized to perform survival analysis, and Enrichr database was introduced to conduct functional enrichment analysis. Hub genes were identified through STRING and Cytoscape. qRT-PCR, luciferase reporter assay, cell counting assay and colony formation assay were performed to validate in silico analytic results.
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Up-regulation of SPC25 promotes breast cancer

Qian Wang, Yanhui Zhu, Zhouxiao Li, Qian Bu, Tong Sun, Hanjin Wang, Handong Sun, Xiufeng Cao,

https://doi.org/10.18632/aging.102153 pp 5689—5704

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Wang Q, Zhu Y, Li Z, Bu Q, Sun T, Wang H, Sun H, Cao X, . Up-regulation of SPC25 promotes breast cancer. . 11:5689-5704. https://doi.org/10.18632/aging.102153

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                TY  - JOUR
                AU  - Wang, Qian 
                AU  - Zhu, Yanhui 
                AU  - Li, Zhouxiao 
                AU  - Bu, Qian 
                AU  - Sun, Tong 
                AU  - Wang, Hanjin 
                AU  - Sun, Handong 
                AU  - Cao, Xiufeng 
                TI  - Up-regulation of SPC25 promotes breast cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102153
                DO  - 10.18632/aging.102153
                SP  - 5689
                EP  - 5704
                PY  - 
                AB  - In this study, expression of the SPC25 gene was characterized in breast cancer (BC), and its effects on BC development and progression, functions in BC cells, and potential underlying mechanisms were examined. Data from TCGAportal and FIREBROWSE indicated that SPC25 was upregulated in BC tissues compared to normal tissues, and CANCERTOOL indicated that higher SPC25 mRNA levels were associated with increased probability of recurrence and poorer survival in BC patients. BC patients with higher SPC25 expression displayed shorter distant metastasis-free survival, relapse-free survival, and overall survival. Colony formation and CCK-8 experiments confirmed that SPC25 promoted proliferation of BC cells. Single-cell analysis indicated that SPC25 is associated with cell cycle regulation, DNA damage and repair, and BC cell proliferation. SPC25 knockdown suppressed proliferation of BC cells. MiRNAs, circRNAs, RNA-binding proteins, transcription factors, and immune factors that might interact with SPC25 mRNA to promote BC were also identified. These findings suggest that SPC25 levels are higher in more malignant BC subtypes and are associated with poor prognosis in BC patients. In addition, DNA methyltransferase inhibitor and transcription factors inhibitor treatments targeting SPC25 might improve survival in BC patients.
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LncRNA ADAMTS9-AS2 inhibits cell proliferation and decreases chemoresistance in clear cell renal cell carcinoma via the miR-27a-3p/FOXO1 axis

Er-lin Song, Li Xing, Liang Wang, Wen-ting Song, Dan-bin Li, Yi Wang, Yi-wei Gu, Ming-ming Liu, Wen-jun Ni, Peng Zhang, Xin Ma, Xu Zhang, Jie Yao, Yang Chen, Rui-hua An,

https://doi.org/10.18632/aging.102154 pp 5705—5725

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Song E, Xing L, Wang L, Song W, Li D, Wang Y, Gu Y, Liu M, Ni W, Zhang P, Ma X, Zhang X, Yao J, et al, . LncRNA ADAMTS9-AS2 inhibits cell proliferation and decreases chemoresistance in clear cell renal cell carcinoma via the miR-27a-3p/FOXO1 axis. . 11:5705-5725. https://doi.org/10.18632/aging.102154

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                TY  - JOUR
                AU  - Song, Er-lin 
                AU  - Xing, Li 
                AU  - Wang, Liang 
                AU  - Song, Wen-ting 
                AU  - Li, Dan-bin 
                AU  - Wang, Yi 
                AU  - Gu, Yi-wei 
                AU  - Liu, Ming-ming 
                AU  - Ni, Wen-jun 
                AU  - Zhang, Peng 
                AU  - Ma, Xin 
                AU  - Zhang, Xu 
                AU  - Yao, Jie 
                AU  - Chen, Yang 
                AU  - An, Rui-hua 
                TI  - LncRNA ADAMTS9-AS2 inhibits cell proliferation and decreases chemoresistance in clear cell renal cell carcinoma via the miR-27a-3p/FOXO1 axis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102154
                DO  - 10.18632/aging.102154
                SP  - 5705
                EP  - 5725
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Song, Er-lin 
                AU  - Xing, Li 
                AU  - Wang, Liang 
                AU  - Song, Wen-ting 
                AU  - Li, Dan-bin 
                AU  - Wang, Yi 
                AU  - Gu, Yi-wei 
                AU  - Liu, Ming-ming 
                AU  - Ni, Wen-jun 
                AU  - Zhang, Peng 
                AU  - Ma, Xin 
                AU  - Zhang, Xu 
                AU  - Yao, Jie 
                AU  - Chen, Yang 
                AU  - An, Rui-hua 
                TI  - LncRNA ADAMTS9-AS2 inhibits cell proliferation and decreases chemoresistance in clear cell renal cell carcinoma via the miR-27a-3p/FOXO1 axis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102154
                DO  - 10.18632/aging.102154
                SP  - 5705
                EP  - 5725
                PY  - 
                AB  - Accumulating evidence reveals the principal role of long noncoding RNAs in the progression of clear cell renal cell carcinoma (ccRCC). However, little is known about the underlying mechanism of ADAM metallopeptidase with thrombospondin type 1 motif, 9 antisense RNA 2 (ADAMTS9-AS2) in ccRCC. Here, bioinformatics analyses verified ADAMTS9-AS2 is a long noncoding RNA and its high expression was associated with better prognosis of ccRCC. ADAMTS9-AS2 was clearly downregulated in ccRCC clinical samples and cell lines. Clinical data showed low-expressed ADAMTS9-AS2 was correlated with worse overall survival in ccRCC patients. Next, miR-27a-3p was identified as an inhibitory target of ADAMTS9-AS2 by dual-luciferase reporter and RNA immunoprecipitation assays. Both overexpressed ADAMTS9-AS2 and underexpressed miR-27a-3p in ccRCC cell lines led to the inhibition of cell proliferation and the reduction of chemoresistance. Additionally, Forkhead Box Protein O1 (FOXO1) was confirmed as the inhibitory target of miR-27a-3p. Induced by ADAMTS9-AS2 overexpression, cell proliferation and chemoresistance exhibited an obvious reduction, FOXO1 expression showed an evident increase, but all were reversed after miR-27a-3p was simultaneously overexpressed. Collectively, these results suggest ADAMTS9-AS2 inhibits the progression and impairs the chemoresistance of ccRCC via miR-27a-3p-mediated regulation of FOXO1 and may serve as a prognostic biomarker and therapeutic target for ccRCC.
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Conserved roles of glucose in suppressing reactive oxygen species-induced cell death and animal survival

Congrong Wang, Yinan Zhang, Fengwen Li, Yuehua Wei,

https://doi.org/10.18632/aging.102155 pp 5726—5743

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Wang C, Zhang Y, Li F, Wei Y, . Conserved roles of glucose in suppressing reactive oxygen species-induced cell death and animal survival. . 11:5726-5743. https://doi.org/10.18632/aging.102155

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                TY  - JOUR
                AU  - Wang, Congrong 
                AU  - Zhang, Yinan 
                AU  - Li, Fengwen 
                AU  - Wei, Yuehua 
                TI  - Conserved roles of glucose in suppressing reactive oxygen species-induced cell death and animal survival
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102155
                DO  - 10.18632/aging.102155
                SP  - 5726
                EP  - 5743
                PY  - 
                AB  - Carbohydrate overconsumption increases blood glucose levels, which contributes to the development of various diseases including obesity and diabetes. It is generally believed that high glucose metabolism increases cellular reactive oxygen species (ROS) levels, damages insulin-secreting cells and leads to age-associated diabetic phenotypes. Here we find that in contrast, high glucose suppresses ROS production induced by paraquat in both mammalian cells and the round worm C. elegans. The role of glucose in suppressing ROS is further supported by glucose&#x2019;s ability to alleviate paraquat&#x2019;s toxicity on C. elegans development. Consistently, we find that the ROS-regulated transcription factor SKN-1 is inactivated by glucose. As a result, the ROS/SKN-1-dependent lifespan extension observed in paraquat-treated animals, mitochondrial respiration mutant isp-1 and germline-less mutant glp-1 are all suppressed by glucose. Our study reveals an unprecedented interaction of glucose with ROS, which could have significant impact on our current understanding of glucose- and ROS-related diseases.
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miR-627-3p inhibits osteosarcoma cell proliferation and metastasis by targeting PTN

Ming He, Peng Shen, Chuang Qiu, Jiashi Wang,

https://doi.org/10.18632/aging.102157 pp 5744—5756

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He M, Shen P, Qiu C, Wang J, . miR-627-3p inhibits osteosarcoma cell proliferation and metastasis by targeting PTN. . 11:5744-5756. https://doi.org/10.18632/aging.102157

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                TY  - JOUR
                AU  - He, Ming 
                AU  - Shen, Peng 
                AU  - Qiu, Chuang 
                AU  - Wang, Jiashi 
                TI  - miR-627-3p inhibits osteosarcoma cell proliferation and metastasis by targeting PTN
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102157
                DO  - 10.18632/aging.102157
                SP  - 5744
                EP  - 5756
                PY  - 
                AB  - Dysregulation of microRNA (miRNA) has been observed in several types of tumors, including osteosarcoma. Biochip analysis was used to identify miRNAs differentially expressed in osteosarcoma tissues. The targeting sites of miR-627-3p were analyzed using miRDB software and fluorescein reporter gene. MTT and Transwell assays were used to analyze the effects of miR-627-3p on the growth and migration of osteosarcoma cells. Western blotting and real-time PCR were used to detect the effects of miR-627-3p on related proteins. In vivo experiments were conducted to verify the effect of miR-627-3p on osteosarcoma. We focused on miR-627-3p because it was the most significantly downregulated miRNA in our screening study. Through luciferase reporter assays, western blotting and real-time PCR we found that miR-627-3p directly targets PTN, and that expression levels of miR-627-3p and PTN are negatively correlated in osteosarcoma cells. Downregulation of miR-627-3p promoted osteosarcoma cell proliferation and metastasis, while its overexpression had the opposite effect. By targeting PTN, miR-627-3p also suppressed expression of Cyclin D1 and MMP2. MiR-627-3p inhibited osteosarcoma metastasis in vivo. Thus, miR-627-3p may be a useful therapeutic target for the treatment osteosarcoma or prevention of metastasis.
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Identification and characterization of telocytes in rat testis

Yifei Liu, Yu Liang, Siyi Wang, Imran Tarique, Waseem Ali Vistro, Haiyan Zhang, Abdul Haseeb, Noor Samad Gandahi, Adeela Iqbal, Tianci An, Huan Yang, Qiusheng Chen, Ping Yang,

https://doi.org/10.18632/aging.102158 pp 5757—5768

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Liu Y, Liang Y, Wang S, Tarique I, Vistro WA, Zhang H, Haseeb A, Gandahi NS, Iqbal A, An T, Yang H, Chen Q, Yang P, . Identification and characterization of telocytes in rat testis. . 11:5757-5768. https://doi.org/10.18632/aging.102158

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                TY  - JOUR
                AU  - Liu, Yifei 
                AU  - Liang, Yu 
                AU  - Wang, Siyi 
                AU  - Tarique, Imran 
                AU  - Vistro, Waseem Ali 
                AU  - Zhang, Haiyan 
                AU  - Haseeb, Abdul 
                AU  - Gandahi, Noor Samad 
                AU  - Iqbal, Adeela 
                AU  - An, Tianci 
                AU  - Yang, Huan 
                AU  - Chen, Qiusheng 
                AU  - Yang, Ping 
                TI  - Identification and characterization of telocytes in rat testis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102158
                DO  - 10.18632/aging.102158
                SP  - 5757
                EP  - 5768
                PY  - 
                AB  - In this study, we investigated the localization, morphological features and cellular interactions of telocytes in the rat testicular interstitium. Transmission electron microscopy (TEM) and immunohistochemical and immunofluorescence analyses of the rat testicular interstitium showed a distinct layer of telocytes surround the seminiferous tubules along with inner layer of peritubular myoid cells. The majority of the telocytes were made up of a small cell body and moniliform prolongations that contained mitochondria and secretory vesicles. Some other telocytes were observed possessing large cell bodies. Within the testicular interstitium, the telocytes formed a network connecting peritubular myoid cells, Leydig cells as well as blood vessels. Immunohistochemical and double immunofluorescence analyses showed that rat testicular telocytes express CD34 and PDGFR&#x3B1;, but are negative for vimentin and &#x3B1;-SMA. Our findings demonstrate the presence of telocytes in the rat testicular interstitium. These cells interact with peritubular myoid cells, seminiferous tubules, Leydig cells and blood vessels via long telopode extensions, which suggests their vital role in the intercellular communication between different cell types within the rat testis.
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The combination of lonafarnib and sorafenib induces cyclin D1 degradation via ATG3-mediated autophagic flux in hepatocellular carcinoma cells

Jialiang Wang, Huan Wei, Yanlin Huang, Dongmei Chen, Guofen Zeng, Yifan Lian, Yuehua Huang,

https://doi.org/10.18632/aging.102165 pp 5769—5785

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Wang J, Wei H, Huang Y, Chen D, Zeng G, Lian Y, Huang Y, . The combination of lonafarnib and sorafenib induces cyclin D1 degradation via ATG3-mediated autophagic flux in hepatocellular carcinoma cells. . 11:5769-5785. https://doi.org/10.18632/aging.102165

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                TY  - JOUR
                AU  - Wang, Jialiang 
                AU  - Wei, Huan 
                AU  - Huang, Yanlin 
                AU  - Chen, Dongmei 
                AU  - Zeng, Guofen 
                AU  - Lian, Yifan 
                AU  - Huang, Yuehua 
                TI  - The combination of lonafarnib and sorafenib induces cyclin D1 degradation via ATG3-mediated autophagic flux in hepatocellular carcinoma cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102165
                DO  - 10.18632/aging.102165
                SP  - 5769
                EP  - 5785
                PY  - 
                AB  - Combination treatment is a promising strategy to improve prognosis of hepatocellular carcinoma (HCC). Sorafenib is a traditional first-line agent approved for the treatment of advanced HCC, though with limited efficacy. Previously, we reported that lonafarnib, an orally bioavailable non-peptide inhibitor targeting farnesyltransferase, synergizes with sorafenib against the growth of HCC cells. In the present study, we aim to clarify the underlying mechanism of this combination strategy. Initially, using in vitro HCC cell model, we confirmed that synergistic treatment of lonafarnib and sorafenib suppressed cell viability and colony formation, and induced cell death. We then found conversion of LC3-I to LC3-II via combination the treatment and observed formation of autophagosomes by electron microscopy. Knockdown of ATG3 inhibited the autophagic flux induced by the combination treatment. Furthermore, we demonstrated that drug-eliciting autophagy selectively promoted the degradation of cyclin D1 in a lysosome-dependent manner and subsequently inhibited DNA synthesis through downregulating the phosphorylation of Rb protein. In conclusion, our results provide a deeper insight into the mechanism for the combination treatment of lonafarnib and sorafenib in HCC therapy.
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A defined human aging phenome

Søren Norge Andreassen, Michael Ben Ezra, Morten Scheibye-Knudsen,

https://doi.org/10.18632/aging.102166 pp 5786—5806

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Andreassen SN, Ben Ezra M, Scheibye-Knudsen M, . A defined human aging phenome. . 11:5786-5806. https://doi.org/10.18632/aging.102166

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                TY  - JOUR
                AU  - Andreassen, Søren Norge 
                AU  - Ben Ezra, Michael 
                AU  - Scheibye-Knudsen, Morten 
                TI  - A defined human aging phenome
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102166
                DO  - 10.18632/aging.102166
                SP  - 5786
                EP  - 5806
                PY  - 
                AB  - Aging is among the most complex phenotypes that occur in humans. Identifying the interplay between different age-associated features is undoubtedly critical to our understanding of aging and thus age-associated diseases. Nevertheless, what constitutes human aging is not well characterized. Towards this end, we mined millions of PubMed abstracts for age-associated terms, enabling us to generate a detailed description of the human aging phenotype. We discovered age-associated features in clusters that can be broadly associated with previously defined hallmarks of aging, consequently identifying areas where interventions could be pursued. Importantly, we validated the newly discovered features by manually verifying the prevalence of these features in combined cohorts describing 76 million individuals, allowing us to stratify features in aging that appear to be the most prominent. In conclusion, we propose a comprehensive landscape of human aging: the human aging phenome.
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Association between healthy vascular aging and the risk of the first stroke in a community-based Chinese cohort

Yingying Yang, Anxin Wang, Xiaodong Yuan, Quanhui Zhao, Xiaoxue Liu, Shuohua Chen, Xiuyan Wang, Yongjun Wang, Shouling Wu, Yilong Wang,

https://doi.org/10.18632/aging.102170 pp 5807—5816

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Yang Y, Wang A, Yuan X, Zhao Q, Liu X, Chen S, Wang X, Wang Y, Wu S, Wang Y, . Association between healthy vascular aging and the risk of the first stroke in a community-based Chinese cohort. . 11:5807-5816. https://doi.org/10.18632/aging.102170

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                TY  - JOUR
                AU  - Yang, Yingying 
                AU  - Wang, Anxin 
                AU  - Yuan, Xiaodong 
                AU  - Zhao, Quanhui 
                AU  - Liu, Xiaoxue 
                AU  - Chen, Shuohua 
                AU  - Wang, Xiuyan 
                AU  - Wang, Yongjun 
                AU  - Wu, Shouling 
                AU  - Wang, Yilong 
                TI  - Association between healthy vascular aging and the risk of the first stroke in a community-based Chinese cohort
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102170
                DO  - 10.18632/aging.102170
                SP  - 5807
                EP  - 5816
                PY  - 
                AB  - In this study we tested whether vascular aging is associated with the risk of first stroke in the Kailuan cohort, a community-based Chinese cohort. For participants aged &#x2265; 50 years, healthy vascular aging (HVA) was defined as an absence of hypertension and a brachial-ankle pulse wave velocity &lt; the mean + 2 standard deviations, which was determined from a reference sample of healthy participants aged &lt; 30 years. The primary outcome was first stroke (ischemic or hemorrhagic). In total, 11,474 participants were enrolled. The prevalence of HVA decreased from 36.0% in participants aged 50-59 years to 4.7% in those aged &#x2265; 70 years. During a median follow-up of 3.3 years, the incidence of first stroke was 0.5% in the HVA group but was 2.6% in the Non-HVA group. After adjusting for confounding variables, HVA was associated with a 0.32-fold lower risk of first stroke compared to the Non-HVA group (95% confidence interval, 0.18-0.56; p &lt; 0.001). It thus appears that HVA reduced the risk of first stroke in a community-based Chinese population. This suggests that evaluation of vascular aging as part of public health screening may be useful for stroke risk assessment.
                ER  -

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The senescence-associated secretory phenotype (SASP) from mesenchymal stromal cells impairs growth of immortalized prostate cells but has no effect on metastatic prostatic cancer cells

Nicola Alessio, Domenico Aprile, Tiziana Squillaro, Giovanni Di Bernardo, Mauro Finicelli, Mariarosa AB Melone, Gianfranco Peluso, Umberto Galderisi,

https://doi.org/10.18632/aging.102172 pp 5817—5828

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Alessio N, Aprile D, Squillaro T, Di Bernardo G, Finicelli M, Melone MA, Peluso G, Galderisi U, . The senescence-associated secretory phenotype (SASP) from mesenchymal stromal cells impairs growth of immortalized prostate cells but has no effect on metastatic prostatic cancer cells. . 11:5817-5828. https://doi.org/10.18632/aging.102172

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                TY  - JOUR
                AU  - Alessio, Nicola 
                AU  - Aprile, Domenico 
                AU  - Squillaro, Tiziana 
                AU  - Di Bernardo, Giovanni 
                AU  - Finicelli, Mauro 
                AU  - Melone, Mariarosa AB 
                AU  - Peluso, Gianfranco 
                AU  - Galderisi, Umberto 
                TI  - The senescence-associated secretory phenotype (SASP) from mesenchymal stromal cells impairs growth of immortalized prostate cells but has no effect on metastatic prostatic cancer cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102172
                DO  - 10.18632/aging.102172
                SP  - 5817
                EP  - 5828
                PY  - 
                AB  - Senescent cells secrete inflammatory cytokines, proteases, and other factors, which are indicated as senescence-associated secretory phenotype (SASP). There are contrasting studies on the role of the SASP in cancer. Studies suggested that cancer cells may misuse the senescent secretome for their growth. Other investigations evidenced that the SASP may induce cancer growth arrest, senescence, or apoptosis. These conflicting data can be reconciled considering that cancer cells can coax senescent cells to secrete factors for their survival, thus abrogating the SASP&#x2019;s anti-cancer effect. Cancer stage may also have an impact on the capacity of the SASP to block tumor proliferation and promote senescence. Indeed, senescence is associated with a permanent cell cycle arrest, which needs functional cell cycle checkpoints. We evaluated the SASP effect on the in vitro biological properties of PNT2 and PC3 cells, which are immortalized prostate cells and metastatic prostatic cancer cells, respectively. We evidenced that SASPs, coming either from mesenchymal stromal cells treated with H202 or with low X-ray doses, induced senescence of immortalized cells but not of cancer cells. Hence, the SASP released by acute senescent cells should be considered as an effective weapon against pre-tumorigenesis events rather than an anti-cancer mechanism acting on malignant cells.
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Long non-coding RNA CASC19 is associated with the progression and prognosis of advanced gastric cancer

Wen-Jie Wang, Chang-An Guo, Rui Li, Zi-Peng Xu, Jian-Ping Yu, Yan Ye, Jun Zhao, Jing Wang, Wen-An Wang, An Zhang, Hong-Tao Li, Chen Wang, Hong-Bin Liu,

https://doi.org/10.18632/aging.102190 pp 5829—5847

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Wang W, Guo C, Li R, Xu Z, Yu J, Ye Y, Zhao J, Wang J, Wang W, Zhang A, Li H, Wang C, Liu H, . Long non-coding RNA CASC19 is associated with the progression and prognosis of advanced gastric cancer. . 11:5829-5847. https://doi.org/10.18632/aging.102190

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 TY - JOUR
 AU - Wang, Wen-Jie 
 AU - Guo, Chang-An 
 AU - Li, Rui 
 AU - Xu, Zi-Peng 
 AU - Yu, Jian-Ping 
 AU - Ye, Yan 
 AU - Zhao, Jun 
 AU - Wang, Jing 
 AU - Wang, Wen-An 
 AU - Zhang, An 
 AU - Li, Hong-Tao 
 AU - Wang, Chen 
 AU - Liu, Hong-Bin 
 TI - Long non-coding RNA CASC19 is associated with the progression and prognosis of advanced gastric cancer
 JO - 
 JA - 
 VL - 11
 IS - 15
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102190
 DO - 10.18632/aging.102190
 SP - 5829
 EP - 5847
 PY - 
 AB - Evidence indicates that aberrantly expressed long non-coding RNAs (lncRNAs) are involved in the development and progression of advanced gastric cancer (AGC). Using RNA sequencing data and clinical information obtained from The Cancer Gene Atlas, we combined differential lncRNA expression profiling and weighted gene co-expression network analysis to identify key lncRNAs associated with AGC progression and prognosis. Cancer susceptibility 19 (CASC19) was the top hub lncRNA among the lncRNAs included in the gene module most significantly correlated with AGC&#x2019;s pathological variables. CASC19 was upregulated in AGC clinical samples and was significantly associated with higher pathologic TNM stage, pathologic T stage, lymph node metastasis, and poor overall survival. Multivariable Cox analysis confirmed that CASC19 overexpression is an independent prognostic factor for overall survival. Furthermore, quantitative real-time PCR assay confirmed that CASC19 expression in four human gastric cancer cells (AGS, BGC-823, MGC-803, and HGC-27) was significantly upregulated compared with human normal gastric mucosal epithelial cell line (GES-1). Functionally, CASC19 knockdown inhibited GC cell proliferation and migration in vitro. These findings suggest that CASC19 may be a novel prognostic biomarker and a potential therapeutic target for AGC.
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Sodium cantharidate targets STAT3 and abrogates EGFR inhibitor resistance in osteosarcoma

Xiang Lu Ji, Ming He,

https://doi.org/10.18632/aging.102193 pp 5848—5863

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Ji XL, He M, . Sodium cantharidate targets STAT3 and abrogates EGFR inhibitor resistance in osteosarcoma. . 11:5848-5863. https://doi.org/10.18632/aging.102193

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                TY  - JOUR
                AU  - Ji, Xiang Lu 
                AU  - He, Ming 
                TI  - Sodium cantharidate targets STAT3 and abrogates EGFR inhibitor resistance in osteosarcoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 15
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102193
                DO  - 10.18632/aging.102193
                SP  - 5848
                EP  - 5863
                PY  - 
                AB  - Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. Overactive EGFR signaling is frequently seen in osteosarcoma cells, and represents a potential therapeutic target. However, feedback activation of STAT3 after EGFR inhibition is linked to treatment resistance, suggesting that combined EGFR/STAT3 inhibition may be needed to overcome this effect. Cantharidin and its analogues have shown strong anticancer effects, including STAT3 inhibition, in several tumor cells. Therefore, we investigated the effects of sodium cantharidate (SC), either as monotherapy and in combination with the EGFR inhibitor erlotinib, on STAT3 activation and osteosarcoma cell growth. Cell viability, migration, and apoptosis assays were performed in human MG63 and U2OS cells, and MG63 xenografts were generated in nude mice to verify the suppression of tumor growth in vivo. Additionally, western blotting and immunohistochemistry were used to verify the STAT3 and EGFR phosphorylation statuses in xenografts. We found that SC repressed cell viability and migration and induced apoptosis in vitro, while combined SC and erlotinib treatment enhanced osteosarcoma growth suppression by preventing feedback activation of STAT3. These data support further development of cantharidin-based combination therapies for metastatic and recurrent/refractory osteosarcoma.
                ER  -

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Volume 11, Issue 15

About the Cover

Editorials

Haili Tian, Peijie Chen, Jun Ren,

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Ioannis P. Trougakos,

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Charlotte K. Boughton, Lia Bally, Roman Hovorka,

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Amy E. Elias, Jill A. Kreiling,

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Niamh M. C. Connolly, Pierre Theurey, Paola Pizzo,

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Patricia Corrales, Marina Martín-Taboada, Gema Medina-Gomez,

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Research Papers

Lei Yu, Si Gui, Yawei Liu, Xiaoyu Qiu, Guozhong Zhang, Xi’an Zhang, Jun Pan, Jun Fan, Songtao Qi, Binghui Qiu,

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Francisco J. Amaro-Gahete, Alejandro De-la-O, Lucas Jurado-Fasoli, Jonatan R. Ruiz, Manuel J. Castillo,

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Yi Liu, Chunpeng Liu, Ankui Zhang, Shichang Yin, Ting Wang, Yan Wang, Meiming Wang, Yixin Liu, Qiaohui Ying, Jinrui Sun, Fulan Wei, Dongxu Liu, Chunling Wang, Shaohua Ge,

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Wen Guo, Qing Yu, Ming Zhang, Fang Li, Yu Liu, Weiwei Jiang, Haitao Jiang, Haijun Li,

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Linfeng Qian, Shaobo Pan, Liping Shi, Yongyi Zhou, Lai Sun, Zhedong Wan, Yufang Ding, Jia Qian,

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Thomas D.W. Wilcockson, Diako Mardanbegi, Baiqiang Xia, Simon Taylor, Pete Sawyer, Hans W. Gellersen, Ira Leroi, Rebecca Killick, Trevor J. Crawford,

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Aleksandra Rosiak-Gill, Kamil Gill, Joanna Jakubik, Monika Fraczek, Lukasz Patorski, Dariusz Gaczarzewicz, Rafał Kurzawa, Maciej Kurpisz, Malgorzata Piasecka,

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Fasil Tekola-Ayele, Tsegaselassie Workalemahu, Gezahegn Gorfu, Deepika Shrestha, Benjamin Tycko, Ronald Wapner, Cuilin Zhang, Germaine M. Buck Louis,

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Kai-Xin Dou, Can Zhang, Chen-Chen Tan, Wei Xu, Jie-Qiong Li, Xi-Peng Cao, Lan Tan, Jin-Tai Yu, for the Alzheimer’s Disease Neuroimaging Initiative (ADNI),

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Laura A. Henze, Trang T.D. Luong, Beate Boehme, Jaber Masyout, Markus P. Schneider, Sebastian Brachs, Florian Lang, Burkert Pieske, Andreas Pasch, Kai-Uwe Eckardt, Jakob Voelkl, Ioana Alesutan,

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Fangkun Liu, Jing Huang, Yuanyuan Xiong, Shuwang Li, Zhixiong Liu,

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Xiaoping Zhong, Anna Kan, Wancong Zhang, Jianda Zhou, Huayong Zhang, Jiasheng Chen, Shijie Tang,

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Sarah W. Curtis, Dawayland O. Cobb, Varun Kilaru, Metrecia L. Terrell, M. Elizabeth Marder, Dana Boyd Barr, Carmen J. Marsit, Michele Marcus, Karen N. Conneely, Alicia K. Smith,

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