Volume 10, Issue 6

Wang H, Zhang Z, Gems D, . Monsters in the uterus: teratoma-like tumors in senescent C. elegans result from a parthenogenetic quasi-program. Aging (Albany NY). 2018 Jun 1910:1188-1189. https://doi.org/10.18632/aging.101486

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PACS-2 functions in colorectal cancer

Marie Kveiborg, Gary Thomas,

https://doi.org/10.18632/aging.101489 pp 1190—1191

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Identification of proteins potentially associated with renal aging in rats

Diangeng Li, Delong Zhao, Weiguang Zhang, Qian Ma, Dong Liu, Qi Huang, Ying Zheng, Xueyuan Bai, Xuefeng Sun, Xiangmei Chen,

https://doi.org/10.18632/aging.101460 pp 1192—1205

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Li D, Zhao D, Zhang W, Ma Q, Liu D, Huang Q, Zheng Y, Bai X, Sun X, Chen X, . Identification of proteins potentially associated with renal aging in rats. Aging (Albany NY). 2018 Jun 1410:1192-1205. https://doi.org/10.18632/aging.101460

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                TY  - JOUR
                AU  - Li, Diangeng 
                AU  - Zhao, Delong 
                AU  - Zhang, Weiguang 
                AU  - Ma, Qian 
                AU  - Liu, Dong 
                AU  - Huang, Qi 
                AU  - Zheng, Ying 
                AU  - Bai, Xueyuan 
                AU  - Sun, Xuefeng 
                AU  - Chen, Xiangmei 
                TI  - Identification of proteins potentially associated with renal aging in rats
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101460
                DO  - 10.18632/aging.101460
                SP  - 1192
                EP  - 1205
                PY  - 
                AB  - We established a young (Y)-old (O) rat kidney transplantation model. With this model, we detected no age-related differences in renal structure between Y→Y and Y→O kidneys or O→O and O→Y kidneys. However, we did detect differences in levels of the senescence markers β-gal and p16 as well as the inflammatory cytokines TNF-α and IL-1β. Using proteomics analysis we detected 66 proteins associated with suppression of aging and 73 proteins associated with enhancement of aging. After construction of a protein-protein interaction network, a total of 73 nodes and 99 edges were analyzed using MCODE, and three significant modules were selected. GO and KEGG analyses showed that these proteins were mainly located in mitochondria and were largely related to oxidative stress. Among them, SOD1 expression was lower in Y→O than Y→Y kidneys and higher in O→Y than O→O kidneys. Acetylated (Ac)-NF-κB showed the opposite expression profile. In addition, SOD1 expression was higher in primary tubular epithelial cells from young rats than old rats, and SOD1 knockdown led to increased Ac-NF-κB expression. These findings suggest the local renal environment, particularly oxidative stress/mitochondrial function, affects renal aging.
                ER  -

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The correlation of copy number variations with longevity in a genome-wide association study of Han Chinese

Xin Zhao, Xiaomin Liu, Aiping Zhang, Huashuai Chen, Qing Huo, Weiyang Li, Rui Ye, Zhihua Chen, Liping Liang, Qiong A. Liu, Juan Shen, Xin Jin, Wenwen Li, Marianne Nygaard, Xiao Liu, Yong Hou, Ting Ni, Lars Bolund, William Gottschalk, Wei Tao, Jun Gu, Xiao-Li Tian, Huanming Yang, Jian Wang, Xun Xu, Michael W. Lutz, Junxia Min, Yi Zeng, Chao Nie,

https://doi.org/10.18632/aging.101461 pp 1206—1222

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Zhao X, Liu X, Zhang A, Chen H, Huo Q, Li W, Ye R, Chen Z, Liang L, Liu QA, Shen J, Jin X, Li W, et al, . The correlation of copy number variations with longevity in a genome-wide association study of Han Chinese. Aging (Albany NY). 2018 Jun 510:1206-1222. https://doi.org/10.18632/aging.101461

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                TY  - JOUR
                AU  - Zhao, Xin 
                AU  - Liu, Xiaomin 
                AU  - Zhang, Aiping 
                AU  - Chen, Huashuai 
                AU  - Huo, Qing 
                AU  - Li, Weiyang 
                AU  - Ye, Rui 
                AU  - Chen, Zhihua 
                AU  - Liang, Liping 
                AU  - Liu, Qiong A. 
                AU  - Shen, Juan 
                AU  - Jin, Xin 
                AU  - Li, Wenwen 
                AU  - Nygaard, Marianne 
                AU  - Liu, Xiao 
                AU  - Hou, Yong 
                AU  - Ni, Ting 
                AU  - Bolund, Lars 
                AU  - Gottschalk, William 
                AU  - Tao, Wei 
                AU  - Gu, Jun 
                AU  - Tian, Xiao-Li 
                AU  - Yang, Huanming 
                AU  - Wang, Jian 
                AU  - Xu, Xun 
                AU  - Lutz, Michael W. 
                AU  - Min, Junxia 
                AU  - Zeng, Yi 
                AU  - Nie, Chao 
                TI  - The correlation of copy number variations with longevity in a genome-wide association study of Han Chinese
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101461
                DO  - 10.18632/aging.101461
                SP  - 1206
                EP  - 1222
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Zhao, Xin 
                AU  - Liu, Xiaomin 
                AU  - Zhang, Aiping 
                AU  - Chen, Huashuai 
                AU  - Huo, Qing 
                AU  - Li, Weiyang 
                AU  - Ye, Rui 
                AU  - Chen, Zhihua 
                AU  - Liang, Liping 
                AU  - Liu, Qiong A. 
                AU  - Shen, Juan 
                AU  - Jin, Xin 
                AU  - Li, Wenwen 
                AU  - Nygaard, Marianne 
                AU  - Liu, Xiao 
                AU  - Hou, Yong 
                AU  - Ni, Ting 
                AU  - Bolund, Lars 
                AU  - Gottschalk, William 
                AU  - Tao, Wei 
                AU  - Gu, Jun 
                AU  - Tian, Xiao-Li 
                AU  - Yang, Huanming 
                AU  - Wang, Jian 
                AU  - Xu, Xun 
                AU  - Lutz, Michael W. 
                AU  - Min, Junxia 
                AU  - Zeng, Yi 
                AU  - Nie, Chao 
                TI  - The correlation of copy number variations with longevity in a genome-wide association study of Han Chinese
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101461
                DO  - 10.18632/aging.101461
                SP  - 1206
                EP  - 1222
                PY  - 
                AB  - Copy number variations (CNVs) have been shown to cause numerous diseases, however, their roles in human lifespan remain elusive. In this study, we investigate the association of CNVs with longevity by comparing the Han Chinese genomes of long-lived individuals from 90 to 117 years of age and the middle-aged from 30 to 65. Our data demonstrate that the numbers of CNVs, especially deletions, increase significantly in a direct correlation with longevity. We identify eleven CNVs that strongly associate with longevity; four of them locate in the chromosome bands, 7p11.2, 20q13.33, 19p12 and 8p23.3 and overlap partially with the CNVs identified in long-lived Danish or U.S. populations, while the other seven have not been reported previously. These CNV regions encode nineteen known genes, and some of which have been shown to affect aging-related phenotypes such as the shortening of telomere length (ZNF208), the risk of cancer (FOXA1, LAMA5, ZNF716), and vascular and immune-related diseases (ARHGEF10, TOR2A, SH2D3C). In addition, we found several pathways enriched in long-lived genomes, including FOXA1 and FOXA transcription factor networks involved in regulating aging or age-dependent diseases such as cancer. Thus, our study has identified longevity-associated CNV regions and their affected genes and pathways. Our results suggest that the human genome structures such as CNVs might play an important role in determining a long life in human.
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Inactivation of hepatic ATRX in Atrx Foxg1cre mice prevents reversal of aging-like phenotypes by thyroxine

Megan E. Rowland, Yan Jiang, Frank Beier, Nathalie G. Bérubé,

https://doi.org/10.18632/aging.101462 pp 1223—1238

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Rowland ME, Jiang Y, Beier F, Bérubé NG, . Inactivation of hepatic ATRX in Atrx Foxg1cre mice prevents reversal of aging-like phenotypes by thyroxine. Aging (Albany NY). 2018 Jun 710:1223-1238. https://doi.org/10.18632/aging.101462

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Provider: 
 TY - JOUR
 AU - Rowland, Megan E. 
 AU - Jiang, Yan 
 AU - Beier, Frank 
 AU - Bérubé, Nathalie G. 
 TI - Inactivation of hepatic ATRX in Atrx Foxg1cre mice prevents reversal of aging-like phenotypes by thyroxine
 JO - 
 JA - Aging (Albany NY)
 VL - 10
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101462
 DO - 10.18632/aging.101462
 SP - 1223
 EP - 1238
 PY - 
 AB - ATRX is an ATP-dependent chromatin remodeler required for the maintenance of genomic integrity. We previously reported that conditional Atrx ablation in the mouse embryonic forebrain and anterior pituitary using the Foxg1cre driver causes reduced health and lifespan. In these mice, premature aging-like phenotypes were accompanied by low circulating levels of insulin-like growth factor 1 (IGF-1) and thyroxine (T4), hormones that maintain stem cell pools and normal metabolic profiles, respectively. Based on emerging evidence that T4 stimulates expression of IGF-1 in pre-pubertal mice, we tested whether T4 supplementation in Atrx Foxg1cre mice could restore IGF-1 levels and ameliorate premature aging-like phenotypes. Despite restoration of normal serum T4 levels, we did not observe improvements in circulating IGF-1. In the liver, thyroid hormone target genes were differentially affected upon T4 treatment, with Igf1 and several other thyroid hormone responsive genes failing to recover normal expression levels. These findings hinted at Cre-mediated Atrx inactivation in the liver of Atrx Foxg1cre mice, which we confirmed. We conclude that the phenotypes observed in the Atrx Foxg1cre mice can be explained in part by a role of ATRX in the liver to promote T4-mediated Igf1 expression, thus explaining the inefficacy of T4 therapy observed in this study.
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Mitochondrial peptides modulate mitochondrial function during cellular senescence

Su-Jeong Kim, Hemal H. Mehta, Junxiang Wan, Chisaka Kuehnemann, Jingcheng Chen, Ji-Fan Hu, Andrew R. Hoffman, Pinchas Cohen,

https://doi.org/10.18632/aging.101463 pp 1239—1256

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Kim S, Mehta HH, Wan J, Kuehnemann C, Chen J, Hu J, Hoffman AR, Cohen P, . Mitochondrial peptides modulate mitochondrial function during cellular senescence. Aging (Albany NY). 2018 Jun 1010:1239-1256. https://doi.org/10.18632/aging.101463

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Provider: 
                TY  - JOUR
                AU  - Kim, Su-Jeong 
                AU  - Mehta, Hemal H. 
                AU  - Wan, Junxiang 
                AU  - Kuehnemann, Chisaka 
                AU  - Chen, Jingcheng 
                AU  - Hu, Ji-Fan 
                AU  - Hoffman, Andrew R. 
                AU  - Cohen, Pinchas 
                TI  - Mitochondrial peptides modulate mitochondrial function during cellular senescence
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101463
                DO  - 10.18632/aging.101463
                SP  - 1239
                EP  - 1256
                PY  - 
                AB  - Cellular senescence is a complex cell fate response that is thought to underlie several age-related pathologies. Despite a loss of proliferative potential, senescent cells are metabolically active and produce energy-consuming effectors, including senescence-associated secretory phenotypes (SASPs). Mitochondria play crucial roles in energy production and cellular signaling, but the key features of mitochondrial physiology and particularly of mitochondria-derived peptides (MDPs), remain underexplored in senescence responses. Here, we used primary human fibroblasts made senescent by replicative exhaustion, doxorubicin or hydrogen peroxide treatment, and examined the number of mitochondria and the levels of mitochondrial respiration, mitochondrial DNA methylation and the mitochondria-encoded peptides humanin, MOTS-c, SHLP2 and SHLP6. Senescent cells showed increased numbers of mitochondria and higher levels of mitochondrial respiration, variable changes in mitochondrial DNA methylation, and elevated levels of humanin and MOTS-c. Humanin and MOTS-c administration modestly increased mitochondrial respiration and selected components of the SASP in doxorubicin-induced senescent cells partially via JAK pathway. Targeting metabolism in senescence cells is an important strategy to reduce SASP production for eliminating the deleterious effects of senescence. These results provide insight into the role of MDPs in mitochondrial energetics and the production of SASP components by senescent cells.
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Abnormal gut microbiota composition contributes to cognitive dysfunction in SAMP8 mice

Gaofeng Zhan, Ning Yang, Shan Li, Niannian Huang, Xi Fang, Jie Zhang, Bin Zhu, Ling Yang, Chun Yang, Ailin Luo,

https://doi.org/10.18632/aging.101464 pp 1257—1267

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Zhan G, Yang N, Li S, Huang N, Fang X, Zhang J, Zhu B, Yang L, Yang C, Luo A, . Abnormal gut microbiota composition contributes to cognitive dysfunction in SAMP8 mice. Aging (Albany NY). 2018 Jun 1010:1257-1267. https://doi.org/10.18632/aging.101464

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                TY  - JOUR
                AU  - Zhan, Gaofeng 
                AU  - Yang, Ning 
                AU  - Li, Shan 
                AU  - Huang, Niannian 
                AU  - Fang, Xi 
                AU  - Zhang, Jie 
                AU  - Zhu, Bin 
                AU  - Yang, Ling 
                AU  - Yang, Chun 
                AU  - Luo, Ailin 
                TI  - Abnormal gut microbiota composition contributes to cognitive dysfunction in SAMP8 mice
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101464
                DO  - 10.18632/aging.101464
                SP  - 1257
                EP  - 1267
                PY  - 
                AB  - Alzheimer’s disease is characterized by cognitive dysfunction and aging is an important predisposing factor; however, the pathological and therapeutic mechanisms are not fully understood. Recently, the role of gut microbiota in Alzheimer’s disease has received increasing attention. The cognitive function in senescence-accelerated mouse prone 8 (SAMP8) mice was significantly decreased and the Chao 1 and Shannon indices, principal coordinates analysis, and principal component analysis results were notably abnormal compared with that of those in senescence-accelerated mouse resistant 1 (SAMR1) mice. Moreover, 27 gut bacteria at six phylogenetic levels differed between SAMP8 and SAMR1 mice. In a separate study, we transplanted fecal bacteria from SAMP8 or SAMR1 mice into pseudo germ-free mice. Interestingly, the pseudo germ-free mice had significantly lower cognitive function prior to transplant. Pseudo germ-free mice that received fecal bacteria transplants from SAMR1 mice but not from SAMP8 mice showed improvements in behavior and in α-diversity and β-diversity indices. In total, 14 bacteria at six phylogenetic levels were significantly altered by the gut microbiota transplant. These results suggest that cognitive dysfunction in SAMP8 mice is associated with abnormal composition of the gut microbiota. Thus, improving abnormal gut microbiota may provide an alternative treatment for cognitive dysfunction and Alzheimer’s disease.
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Age-related M1/M2 phenotype changes in circulating monocytes from healthy/unhealthy individuals

Andrea Costantini, Nadia Viola, Antonella Berretta, Roberta Galeazzi, Giulia Matacchione, Jacopo Sabbatinelli, Gianluca Storci, Serena De Matteis, Luca Butini, Maria Rita Rippo, Antonio Domenico Procopio, Daniele Caraceni, Roberto Antonicelli, Fabiola Olivieri, Massimiliano Bonafè,

https://doi.org/10.18632/aging.101465 pp 1268—1280

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Costantini A, Viola N, Berretta A, Galeazzi R, Matacchione G, Sabbatinelli J, Storci G, De Matteis S, Butini L, Rippo MR, Procopio AD, Caraceni D, Antonicelli R, et al, . Age-related M1/M2 phenotype changes in circulating monocytes from healthy/unhealthy individuals. Aging (Albany NY). 2018 Jun 810:1268-1280. https://doi.org/10.18632/aging.101465

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                TY  - JOUR
                AU  - Costantini, Andrea 
                AU  - Viola, Nadia 
                AU  - Berretta, Antonella 
                AU  - Galeazzi, Roberta 
                AU  - Matacchione, Giulia 
                AU  - Sabbatinelli, Jacopo 
                AU  - Storci, Gianluca 
                AU  - De Matteis, Serena 
                AU  - Butini, Luca 
                AU  - Rippo, Maria Rita 
                AU  - Procopio, Antonio Domenico 
                AU  - Caraceni, Daniele 
                AU  - Antonicelli, Roberto 
                AU  - Olivieri, Fabiola 
                AU  - Bonafè, Massimiliano 
                TI  - Age-related M1/M2 phenotype changes in circulating monocytes from healthy/unhealthy individuals
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101465
                DO  - 10.18632/aging.101465
                SP  - 1268
                EP  - 1280
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Costantini, Andrea 
                AU  - Viola, Nadia 
                AU  - Berretta, Antonella 
                AU  - Galeazzi, Roberta 
                AU  - Matacchione, Giulia 
                AU  - Sabbatinelli, Jacopo 
                AU  - Storci, Gianluca 
                AU  - De Matteis, Serena 
                AU  - Butini, Luca 
                AU  - Rippo, Maria Rita 
                AU  - Procopio, Antonio Domenico 
                AU  - Caraceni, Daniele 
                AU  - Antonicelli, Roberto 
                AU  - Olivieri, Fabiola 
                AU  - Bonafè, Massimiliano 
                TI  - Age-related M1/M2 phenotype changes in circulating monocytes from healthy/unhealthy individuals
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101465
                DO  - 10.18632/aging.101465
                SP  - 1268
                EP  - 1280
                PY  - 
                AB  - Macrophage polarization is a candidate biomarker of disease-related inflammatory status, but its modulation during aging has not been investigated. To do this, the M1/M2 profile was assessed by CD80/CD163 gating in classical (CD14++CD16-), intermediate (CD14++CD16+), and non-classical (CD14lowCD16+) monocytes from 31 healthy subjects (CTRs) of different ages. Cytofluorimetric analysis showed a significantly different CD80/CD163 distribution in the three subsets, as more than 80% of classical and intermediate monocytes were CD80+CD163+, whereas most non-classical monocytes were CD80-CD163- and CD163+. Non-classical CD163+ monocytes were significantly higher whereas classical CD163+ and CD80-CD163- monocytes significantly lower in older than younger CTRs (cut-off, 65 years), suggesting different age-related trends for M2 subsets. To establish whether an M1/M2 imbalance could be associated with disease, 21 patients with acute myocardial infarction (AMI) were compared with older CTRs. The AMI patients showed a significantly decreased proportion of CD163+CD80+ and an increased proportion of CD163+ and CD163-CD80- cells among classical monocytes, opposite trends to those observed in healthy aging. Moreover, a significantly greater proportion of intermediate and non-classical CD80+ monocytes suggested a shift to a pro-inflammatory phenotype. Overall, CD163/CD80 cytofluorimetric characterization of circulating monocytes provides additional information about their polarization and could be an innovative tool to monitor aging.
                ER  -

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CircSNCA downregulation by pramipexole treatment mediates cell apoptosis and autophagy in Parkinson’s disease by targeting miR-7

Qiuling Sang, Xiaoyang Liu, Libo Wang, Ling Qi, Wenping Sun, Weiyao Wang, Yajuan Sun, Haina Zhang,

https://doi.org/10.18632/aging.101466 pp 1281—1293

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Sang Q, Liu X, Wang L, Qi L, Sun W, Wang W, Sun Y, Zhang H, . CircSNCA downregulation by pramipexole treatment mediates cell apoptosis and autophagy in Parkinson’s disease by targeting miR-7. Aging (Albany NY). 2018 Jun 2810:1281-1293. https://doi.org/10.18632/aging.101466

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                TY  - JOUR
                AU  - Sang, Qiuling 
                AU  - Liu, Xiaoyang 
                AU  - Wang, Libo 
                AU  - Qi, Ling 
                AU  - Sun, Wenping 
                AU  - Wang, Weiyao 
                AU  - Sun, Yajuan 
                AU  - Zhang, Haina 
                TI  - CircSNCA downregulation by pramipexole treatment mediates cell apoptosis and autophagy in Parkinson’s disease by targeting miR-7
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101466
                DO  - 10.18632/aging.101466
                SP  - 1281
                EP  - 1293
                PY  - 
                AB  - We aimed to explore the mechanism of pramipexole (PPX) actions in the treatment of Parkinson’s disease (PD). Genes related to PD and PPX were screened through bioinformatics retrieval. The PD model was constructed by applying 1-methyl-4-phenylpyridinium (MMP+). The RNA expression levels of circSNCA, SNCA, apoptosis-related genes (BCL2, CASP3, BAX, PTEN and P53) and miR-7 were detected by qRT-PCR. Protein expression was determined by western blot. The interactions between circSNCA-miR-7-SNCA were verified by dual luciferase assay and immunofluorescence localization. Cell viability was determined by MTT assay. SNCA and circSNCA expression levels in PD were downregulated after PPX treatment, consistent with the levels of pro-apoptotic genes. CircSNCA increased SNCA expression by downregulating miR-7 in PD as a competitive endogenous RNA (ceRNA). Lower circSNCA expression was associated with the reduced expression of pro-apoptotic (CASP3, BAX, PTEN and P53) proteins. CircSNCA downregulation could decrease apoptosis and induce autophagy in PD. In conclusion, the downregulation of circSNCA by PPX treatment reduced cell apoptosis and promoted cell autophagy in PD via a mechanism that served as a miR-7 sponge to upregulate SNCA.
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MicroRNA-506-3p inhibits osteosarcoma cell proliferation and metastasis by suppressing RAB3D expression

Wang Jiashi, Qiu Chuang, Zhang Zhenjun, Wang Guangbin, Li Bin, He Ming,

https://doi.org/10.18632/aging.101468 pp 1294—1305

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Jiashi W, Chuang Q, Zhenjun Z, Guangbin W, Bin L, Ming H, . MicroRNA-506-3p inhibits osteosarcoma cell proliferation and metastasis by suppressing RAB3D expression. Aging (Albany NY). 2018 Jun 1010:1294-1305. https://doi.org/10.18632/aging.101468

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                TY  - JOUR
                AU  - Jiashi, Wang 
                AU  - Chuang, Qiu 
                AU  - Zhenjun, Zhang 
                AU  - Guangbin, Wang 
                AU  - Bin, Li 
                AU  - Ming, He 
                TI  - MicroRNA-506-3p inhibits osteosarcoma cell proliferation and metastasis by suppressing RAB3D expression
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101468
                DO  - 10.18632/aging.101468
                SP  - 1294
                EP  - 1305
                PY  - 
                AB  - Osteosarcoma is an aggressive bone tumor primarily affecting children and adolescents. Its cause is not yet fully understood, and there is an urgent need for more effective treatment. In the present study we identified several miRNAs whose expression is altered in osteosarcoma compared to adjacent normal tissue. Moreover, expression levels of one of those miRNAs, miR-506-3p, correlated negatively with expression of RAB3D (a Ras-related protein). Suppression of miR-506-3p in osteosarcoma led to increased expression of RAB3D, which in turn led to increased CDK4 (cyclin-dependent kinase 4) and MMP9 (matrix metalloprotein 9) activities. Our results suggest that miR-506-3p acts as a tumor suppressor in osteosarcoma and that its downregulation leads to tumor cell proliferation and metastasis due to upregulation of RAB3D- and CDK4-mediated signaling. miR-506-3p thus appears be a potentially useful target for adjuvant therapy in osteosarcoma patients.
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Loss of NAMPT in aging retinal pigment epithelium reduces NAD⁺ availability and promotes cellular senescence

Ravirajsinh N. Jadeja, Folami L. Powell, Malita A. Jones, Jasmine Fuller, Ethan Joseph, Menaka C. Thounaojam, Manuela Bartoli, Pamela M. Martin,

https://doi.org/10.18632/aging.101469 pp 1306—1323

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Jadeja RN, Powell FL, Jones MA, Fuller J, Joseph E, Thounaojam MC, Bartoli M, Martin PM, . Loss of NAMPT in aging retinal pigment epithelium reduces NAD⁺ availability and promotes cellular senescence. Aging (Albany NY). 2018 Jun 1210:1306-1323. https://doi.org/10.18632/aging.101469

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Provider: 
 TY - JOUR
 AU - Jadeja, Ravirajsinh N. 
 AU - Powell, Folami L. 
 AU - Jones, Malita A. 
 AU - Fuller, Jasmine 
 AU - Joseph, Ethan 
 AU - Thounaojam, Menaka C. 
 AU - Bartoli, Manuela 
 AU - Martin, Pamela M. 
 TI - Loss of NAMPT in aging retinal pigment epithelium reduces NAD+ availability and promotes cellular senescence
 JO - 
 JA - Aging (Albany NY)
 VL - 10
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101469
 DO - 10.18632/aging.101469
 SP - 1306
 EP - 1323
 PY - 
 AB - Retinal pigment epithelium (RPE) performs numerous functions critical to retinal health and visual function. RPE senescence is a hallmark of aging and degenerative retinal disease development. Here, we evaluated the temporal expression of key nicotinamide adenine dinucleotide (NAD+)-biosynthetic genes and associated levels of NAD+, a principal regulator of energy metabolism and cellular fate, in mouse RPE. NAD+ levels declined with age and correlated directly with decreased nicotinamide phosphoribosyltransferase (NAMPT) expression, increased expression of senescence markers (p16INK4a, p21Waf/Cip1, ApoJ, CTGF and β-galactosidase) and significant reductions in SIRT1 expression and activity. We simulated in vitro the age-dependent decline in NAD+ and the related increase in RPE senescence in human (ARPE-19) and mouse primary RPE using the NAMPT inhibitor FK866 and demonstrated the positive impact of NAD+-enhancing therapies on RPE cell viability. This, we confirmed in vivo in the RPE of mice injected sub-retinally with FK866 in the presence or absence of nicotinamide mononucleotide. Our data confirm the importance of NAD+ to RPE cell biology normally and in aging and demonstrate the potential utility of therapies targeting NAMPT and NAD+ biosynthesis to prevent or alleviate consequences of RPE senescence in aging and/or degenerative retinal diseases in which RPE dysfunction is a crucial element.
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Integrated DNA methylation and gene expression analysis identifies SLAMF7 as a key regulator of atherosclerosis

Zhangyong Xia, Mingliang Gu, Xiaodong Jia, Xiaoting Wang, Chunxia Wu, Jiangwen Guo, Liyong Zhang, Yifeng Du, Jiyue Wang,

https://doi.org/10.18632/aging.101470 pp 1324—1337

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Xia Z, Gu M, Jia X, Wang X, Wu C, Guo J, Zhang L, Du Y, Wang J, . Integrated DNA methylation and gene expression analysis identifies SLAMF7 as a key regulator of atherosclerosis. Aging (Albany NY). 2018 Jun 1310:1324-1337. https://doi.org/10.18632/aging.101470

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                TY  - JOUR
                AU  - Xia, Zhangyong 
                AU  - Gu, Mingliang 
                AU  - Jia, Xiaodong 
                AU  - Wang, Xiaoting 
                AU  - Wu, Chunxia 
                AU  - Guo, Jiangwen 
                AU  - Zhang, Liyong 
                AU  - Du, Yifeng 
                AU  - Wang, Jiyue 
                TI  - Integrated DNA methylation and gene expression analysis identifies SLAMF7 as a key regulator of atherosclerosis
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101470
                DO  - 10.18632/aging.101470
                SP  - 1324
                EP  - 1337
                PY  - 
                AB  - Atherosclerosis (AS) is a multifactorial disease. Exploration of DNA methylation in regulating gene transcription in a cell type- and stage-specific manner will shed light on understanding the biological processes associated with plaque stability. We identified 174 up-regulated genes with hypo-methylation in the promoter, and 86 down-regulated genes with hyper-methylation in the promoter, in AS vs. healthy controls. Among them, high expression of signaling lymphocytic activation molecule 7 (SLAM7) was examined in carotid plaque vs. intact tissue, in advanced plaque vs. early atherosclerotic tissue, and SLAMF7 protein expressed significantly higher in the unstable plaques than that in the stable plaques, especially in the CD68-positive macrophages. Depletion of SLAMF7 in plaque-derived macrophages induced a suppressed secretion of proinflammatory cytokines, and inhibited proliferation of vascular smooth muscle cells. These data provide emerging evidence that SLAMF7 could be a target of potential therapeutic intervention in carotid AS.
                ER  -

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Chronic vitamin D insufficiency impairs physical performance in C57BL/6J mice

Kenneth L. Seldeen, Manhui Pang, Merced M. Leiker, Jonathan E. Bard, Maria Rodríguez-Gonzalez, Mireya Hernandez, Zachary Sheridan, Norma Nowak, Bruce R. Troen,

https://doi.org/10.18632/aging.101471 pp 1338—1355

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Seldeen KL, Pang M, Leiker MM, Bard JE, Rodríguez-Gonzalez M, Hernandez M, Sheridan Z, Nowak N, Troen BR, . Chronic vitamin D insufficiency impairs physical performance in C57BL/6J mice. Aging (Albany NY). 2018 Jun 1410:1338-1355. https://doi.org/10.18632/aging.101471

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                TY  - JOUR
                AU  - Seldeen, Kenneth L. 
                AU  - Pang, Manhui 
                AU  - Leiker, Merced M. 
                AU  - Bard, Jonathan E. 
                AU  - Rodríguez-Gonzalez, Maria 
                AU  - Hernandez, Mireya 
                AU  - Sheridan, Zachary 
                AU  - Nowak, Norma 
                AU  - Troen, Bruce R. 
                TI  - Chronic vitamin D insufficiency impairs physical performance in C57BL/6J mice
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101471
                DO  - 10.18632/aging.101471
                SP  - 1338
                EP  - 1355
                PY  - 
                AB  - Vitamin D insufficiency (serum 25-OH vitamin D &lt; 30 ng/ml) affects 70-80% of the general population, yet the long-term impacts on physical performance and the progression of sarcopenia are poorly understood. We therefore followed 6-month-old male C57BL/6J mice (n=6) consuming either sufficient (STD, 1000 IU) or insufficient (LOW, 125 IU) vitamin D3/kg chow for 12 months (equivalent to 20-30 human years). LOW supplemented mice exhibited a rapid decline of serum 25-OH vitamin D levels by two weeks that remained between 11-15 ng/mL for all time points thereafter. After 12 months LOW mice displayed worse grip endurance (34.6 ± 14.1 versus 147.5 ± 50.6 seconds, p=0.001), uphill sprint speed (16.0 ± 1.0 versus 21.8 ± 2.4 meters/min, p=0.0007), and stride length (4.4 ± 0.3 versus 5.1 ± 0.3, p=0.002). LOW mice also showed less lean body mass after 8 months (57.5% ± 5.1% versus 64.5% ± 4.0%, p=0.023), but not after 12 months of supplementation, as well as greater protein expression of atrophy pathway gene atrogin‑1. Additionally, microRNA sequencing revealed differential expression of mIR‑26a in muscle tissue of LOW mice. These data suggest chronic vitamin D insufficiency may be an important factor contributing to functional decline and sarcopenia.
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Aged cells in human skeletal muscle after resistance exercise

Chi Yang, Ying Jiao, Bing Wei, Zeyi Yang, Jin-Fu Wu, Jorgen Jensen, Wei-Horng Jean, Chih-Yang Huang, Chia-Hua Kuo,

https://doi.org/10.18632/aging.101472 pp 1356—1365

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Yang C, Jiao Y, Wei B, Yang Z, Wu J, Jensen J, Jean W, Huang C, Kuo C, . Aged cells in human skeletal muscle after resistance exercise. Aging (Albany NY). 2018 Jun 2710:1356-1365. https://doi.org/10.18632/aging.101472

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                TY  - JOUR
                AU  - Yang, Chi 
                AU  - Jiao, Ying 
                AU  - Wei, Bing 
                AU  - Yang, Zeyi 
                AU  - Wu, Jin-Fu 
                AU  - Jensen, Jorgen 
                AU  - Jean, Wei-Horng 
                AU  - Huang, Chih-Yang 
                AU  - Kuo, Chia-Hua 
                TI  - Aged cells in human skeletal muscle after resistance exercise
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101472
                DO  - 10.18632/aging.101472
                SP  - 1356
                EP  - 1365
                PY  - 
                AB  - It remains unclear how exercise, as an entropic event, brings benefit against human aging. Here we examined longitudinal changes of p16Ink4a+ senescent cells in skeletal muscle of young men (aged 22.5&#xB1;1.7 y) before and after resistance exercise (0 h and 48 h) with multiple biopsies at two different protein availabilities: low protein (14%) and isocaloric high protein (44%) supplemented conditions. Immunohistochemistry analysis of muscle cross-sections using p16Ink4a and CD34 antibodies confirmed that the detected senescent cells were endothelial progenitor cells. Leukocyte infiltration into skeletal muscle increased during resistance exercise. The senescent cells in muscle decreased (-48%, P &lt; 0.01) after exercise for 48 h. Low protein supplementation resulted in greater infiltrations of both CD68+ phagocytic macrophage and leukocyte, further decreased p16Ink4a+ senescent cells (-73%, P &lt; 0.001), and delayed increases in regenerative CD163+ macrophage in skeletal muscle, compared with high protein supplemented condition. Significant gain in muscle mass after 12 weeks of training occurred only under high protein supplemented condition. Conclusion: Rapid senescent cell clearance of human skeletal muscle during resistance exercise seems to associate with enhanced in situ phagocytosis. High protein availability accelerates resolution of muscle inflammation and promotes muscle increment after training.
                ER  -

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A panel of three oxidative stress-related genes predicts overall survival in ovarian cancer patients received platinum-based chemotherapy

Jin Zhang, Lixiao Yang, Xiaohong Xiang, Zhuoying Li, Kai Qu, Ke Li,

https://doi.org/10.18632/aging.101473 pp 1366—1379

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Zhang J, Yang L, Xiang X, Li Z, Qu K, Li K, . A panel of three oxidative stress-related genes predicts overall survival in ovarian cancer patients received platinum-based chemotherapy. Aging (Albany NY). 2018 Jun 1710:1366-1379. https://doi.org/10.18632/aging.101473

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                TY  - JOUR
                AU  - Zhang, Jin 
                AU  - Yang, Lixiao 
                AU  - Xiang, Xiaohong 
                AU  - Li, Zhuoying 
                AU  - Qu, Kai 
                AU  - Li, Ke 
                TI  - A panel of three oxidative stress-related genes predicts overall survival in ovarian cancer patients received platinum-based chemotherapy
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101473
                DO  - 10.18632/aging.101473
                SP  - 1366
                EP  - 1379
                PY  - 
                AB  - Ovarian cancer yields the highest mortality rate of all lethal gynecologic cancers, and the prognosis is unsatisfactory with the major obstacle in resistance to chemotherapy. The generation of reactive oxygen species (ROS) in tumor tissues was associated with chemotherapeutic effectiveness by mediating cellular longevity. In this study, we screened the prognostic values of oxidative stress-related genes in ovarian cancer patients received platinum-based chemotherapy, and conducted a prognostic gene signature composing of three genes, TXNRD1, GLA and GSTZ1. This three-gene signature was significantly associated with overall survival (OS), but not progression-free survival (PFS), in both training (n=276) and validation cohorts (n=230). Interestingly, we found that the prognostic value of three-gene signature was reinforced in platinum-sensitive patients. Subgroup analysis further suggested that patients with elder age, higher pathological grades and advanced tumor stages in low-risk score group could benefit from platinum-based chemotherapy. Functional analysis showed that the inactivation of several signaling pathways, including cell cycle, insulin-like growth factor 1 (IGF1) /mTOR and Fas pathways, was affected by three genes. Collectively, our results provided evidence that a panel of three oxidative stress-related gene signature had prognostic values for ovarian cancer patients received platinum-based chemotherapy.
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The expression of C1 inhibitor (C1INH) in macrophages is upregulated by retinal pigment epithelial cells – implication in subretinal immune privilege in the aging eye

Chang Luo, Jiawu Zhao, Mei Chen, Heping Xu,

https://doi.org/10.18632/aging.101474 pp 1380—1389

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Luo C, Zhao J, Chen M, Xu H, . The expression of C1 inhibitor (C1INH) in macrophages is upregulated by retinal pigment epithelial cells – implication in subretinal immune privilege in the aging eye. Aging (Albany NY). 2018 Jun 1310:1380-1389. https://doi.org/10.18632/aging.101474

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                TY  - JOUR
                AU  - Luo, Chang 
                AU  - Zhao, Jiawu 
                AU  - Chen, Mei 
                AU  - Xu, Heping 
                TI  - The expression of C1 inhibitor (C1INH) in macrophages is upregulated by retinal pigment epithelial cells – implication in subretinal immune privilege in the aging eye
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101474
                DO  - 10.18632/aging.101474
                SP  - 1380
                EP  - 1389
                PY  - 
                AB  - Age-related para-inflammation in the retina-choroidal interface is featured by low-levels of complement activation and subretinal macrophage accumulation. This study aimed to understand how complement expression in macrophages is regulated by retinal pigment epithelium (RPE). Bone marrow-derived macrophages (BMDMs) and RPE cells were cultured from 8-10 weeks old C57BL/6J mice. The BMDMs were co-cultured with normal RPE, or oxidized photoreceptor outer segment (oxPOS) or TNF-α pre-treated RPE, or apoptotic RPE, or RPE-choroid eyecups. Macrophages were then isolated and processed for real-time RT-PCR. The expression of complement inhibitor C1INH in BMDMs was significantly upregulated by RPE and RPE-choroid eyecups. The eyecups also upregulated CFH, CD59a, and Crry in BMDMs. oxPOS pre-treated RPE upregulated C1qb but down-regulated C3 expression in BMDMs. TNF-α pre-treated RPE enhanced C1INH and CFB expression. When BMDMs were treated with apoptotic RPE, the expression of C1qb, CFH, and CD59a was reduced, whereas the expression of C3, CFB and C1INH was increased. Our results suggest that RPE can modulate macrophages complement expression at the retina-choroidal interface even under aging or oxidative conditions. However, during inflammation, they may promote the alternative pathway of complement activation through down-regulating CFH and CD59a and upregulating CFB and C3.
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Five ETS family members, ELF-1, ETV-4, ETV-3L, ETS-1, and ETS-2 upregulate human leukocyte-associated immunoglobulin-like receptor-1 gene basic promoter activity

Qizhi Cao, Shude Yang, Qing Lv, Yan Liu, Li Li, Xiaojie Wu, Guiwu Qu, Xiaoli He, Xiaoshu Zhang, Shuqin Sun, Boqing Li, Jing An, Tao Hu, Jiangnan Xue,

https://doi.org/10.18632/aging.101475 pp 1390—1401

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Cao Q, Yang S, Lv Q, Liu Y, Li L, Wu X, Qu G, He X, Zhang X, Sun S, Li B, An J, Hu T, et al, . Five ETS family members, ELF-1, ETV-4, ETV-3L, ETS-1, and ETS-2 upregulate human leukocyte-associated immunoglobulin-like receptor-1 gene basic promoter activity. Aging (Albany NY). 2018 Jun 1810:1390-1401. https://doi.org/10.18632/aging.101475

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                TY  - JOUR
                AU  - Cao, Qizhi 
                AU  - Yang, Shude 
                AU  - Lv, Qing 
                AU  - Liu, Yan 
                AU  - Li, Li 
                AU  - Wu, Xiaojie 
                AU  - Qu, Guiwu 
                AU  - He, Xiaoli 
                AU  - Zhang, Xiaoshu 
                AU  - Sun, Shuqin 
                AU  - Li, Boqing 
                AU  - An, Jing 
                AU  - Hu, Tao 
                AU  - Xue, Jiangnan 
                TI  - Five ETS family members, ELF-1, ETV-4, ETV-3L, ETS-1, and ETS-2 upregulate human leukocyte-associated immunoglobulin-like receptor-1 gene basic promoter activity
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101475
                DO  - 10.18632/aging.101475
                SP  - 1390
                EP  - 1401
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Cao, Qizhi 
                AU  - Yang, Shude 
                AU  - Lv, Qing 
                AU  - Liu, Yan 
                AU  - Li, Li 
                AU  - Wu, Xiaojie 
                AU  - Qu, Guiwu 
                AU  - He, Xiaoli 
                AU  - Zhang, Xiaoshu 
                AU  - Sun, Shuqin 
                AU  - Li, Boqing 
                AU  - An, Jing 
                AU  - Hu, Tao 
                AU  - Xue, Jiangnan 
                TI  - Five ETS family members, ELF-1, ETV-4, ETV-3L, ETS-1, and ETS-2 upregulate human leukocyte-associated immunoglobulin-like receptor-1 gene basic promoter activity
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101475
                DO  - 10.18632/aging.101475
                SP  - 1390
                EP  - 1401
                PY  - 
                AB  - Human leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1), an immunoinhibitory receptor, is expressed on most types of hematopoietic cells and some tumor cells. LAIR-1 plays an inhibitory role in immune cell maturation, differentiation, and activation. LAIR-1 is also involved in some autoimmune diseases and tumors. However, the mechanism controlling the regulation of the LAIR-1 gene is still unknown. In order to elucidate the molecular mechanisms involved in LAIR-1 regulation, in the present study, we cloned and characterized the promoter region of LAIR-1 gene using a series of truncated promoter plasmids in luciferase reporter assays. Our results show that the basic core promoter of LAIR-1 is located within the region -256/-8 relative to the translational start site. Our further studies indicate that five ETS transcription factors: ELF-1, ETV-4, ETV-3L, ETS-1 and ETS-2, can up-regulate the LAIR-1 basic promoter activity. Of these, ETS-2 is the most effective transcription factor. Moreover, ETS-2 was confirmed to interact directly with the basic promoter of LAIR-1. This study presents the first description of regions/factors capable of up-regulation the promoter activity of LAIR-1. This new knowledge contributes to understanding of the molecular mechanisms involved in LAIR-1 associated immune regulation and diseases.
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The role of microRNA-608 polymorphism on the susceptibility and survival of cancer: a meta-analysis

Zhi-Ming Dai, Jian-Rui Lv, Kang Liu, Xiao-Ming Lei, Wei Li, Gang Wu, Xing-Han Liu, Yu-Xiao Zhu, Qian Hao, Zhi-Jun Dai,

https://doi.org/10.18632/aging.101476 pp 1402—1414

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Dai Z, Lv J, Liu K, Lei X, Li W, Wu G, Liu X, Zhu Y, Hao Q, Dai Z, . The role of microRNA-608 polymorphism on the susceptibility and survival of cancer: a meta-analysis. Aging (Albany NY). 2018 Jun 1610:1402-1414. https://doi.org/10.18632/aging.101476

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                TY  - JOUR
                AU  - Dai, Zhi-Ming 
                AU  - Lv, Jian-Rui 
                AU  - Liu, Kang 
                AU  - Lei, Xiao-Ming 
                AU  - Li, Wei 
                AU  - Wu, Gang 
                AU  - Liu, Xing-Han 
                AU  - Zhu, Yu-Xiao 
                AU  - Hao, Qian 
                AU  - Dai, Zhi-Jun 
                TI  - The role of microRNA-608 polymorphism on the susceptibility and survival of cancer: a meta-analysis
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101476
                DO  - 10.18632/aging.101476
                SP  - 1402
                EP  - 1414
                PY  - 
                AB  - The role of rs4919510 polymorphism in microRNA-608 (miR-608) and cancer susceptibility and prognosis remain controversial and debatable. We conducted a meta-analysis of twenty-four eligible publications on the association of rs4919510 polymorphism with cancer risk and/or prognosis. Odds ratios, hazard ratios, and 95% confidence interval were used to investigate the association between this polymorphism and susceptibility, overall survival, and recurrence-free survival of cancer. Overall, eighteen case-control studies and nine cohort studies evaluated the susceptibility and prognostic value of rs4919510 polymorphism in cancer, respectively. Pooled analysis showed that rs4919510 polymorphism was not associated with cancer risk in all five genetic models. When stratifying by different cancer sites, rs4919510 polymorphism was detected to have a significant association with a decreased risk of colorectal cancer in homozygous model (P = 0.006) and recessive model (P = 0.001), subgroup analysis also emerged a weakened correlation between rs4919510 polymorphism and an increased risk of papillary thyroid cancer in heterozygote model (P = 0.04). Furthermore, the prognosis of rs4919510 variant in cancer patients showed that rs4919510 GG genotype was significant association with poor recurrence-free survival in homozygous models (P = 0.04). The meta-analysis suggested that the microRNA-608 rs4919510 polymorphism maybe associate with a significantly decreased risk for colorectal cancer. Further investigations on larger populations are required to evaluate and confirm this relationship.
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Induction of neutrophil apoptosis by a Bcl-2 inhibitor reduces particulate matter-induced lung inflammation

Xinwei Geng, Xiaohui Wang, Man Luo, Meichun Xing, Yinfang Wu, Wen Li, Zhihua Chen, Huahao Shen, Songmin Ying,

https://doi.org/10.18632/aging.101477 pp 1415—1423

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Geng X, Wang X, Luo M, Xing M, Wu Y, Li W, Chen Z, Shen H, Ying S, . Induction of neutrophil apoptosis by a Bcl-2 inhibitor reduces particulate matter-induced lung inflammation. Aging (Albany NY). 2018 Jun 2610:1415-1423. https://doi.org/10.18632/aging.101477

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                TY  - JOUR
                AU  - Geng, Xinwei 
                AU  - Wang, Xiaohui 
                AU  - Luo, Man 
                AU  - Xing, Meichun 
                AU  - Wu, Yinfang 
                AU  - Li, Wen 
                AU  - Chen, Zhihua 
                AU  - Shen, Huahao 
                AU  - Ying, Songmin 
                TI  - Induction of neutrophil apoptosis by a Bcl-2 inhibitor reduces particulate matter-induced lung inflammation
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101477
                DO  - 10.18632/aging.101477
                SP  - 1415
                EP  - 1423
                PY  - 
                AB  - BackgroundEnvironmental particulate matter exposure can cause various respiratory problems including aggravated asthma, decreased lung function and increased respiratory symptoms. However, the molecular mechanisms underlying PM-induced lung inflammation are incompletely understood. Effective therapeutic strategies are required.ResultsA mouse model of particulate matter-induced lung inflammation was used to identify the pathology and the molecular mechanisms for particulate matter-induced lung inflammation. The mouse model revealed that particulate matter induced neutrophil-dominated lung inflammation. Neutrophils derived from particulate matter-instilled mice showed decreased apoptosis and elevated Bcl-2 expression. Further studies in vav-Bcl-2 transgenic mice made it clear that Bcl-2 overexpression caused a marked increase in neutrophils in bronchoalveolar lavage fluid. Furthermore, we found that the Bcl-2 inhibitor ABT-199 reduced particulate matter-induced lung inflammation, and induced apoptosis of neutrophils in particulate matter-induced lung inflammation mice model.ConclusionsParticulate matter-induced lung inflammation is mediated in part by inhibition of apoptosis of inflammatory cells. Bcl-2 is responsible for the reduced apoptosis of inflammatory cells in particulate matter-induced lung inflammation. The Bcl-2 selective inhibitor ABT-199 reduces particulate matter-induced lung inflammation by inducing the apoptosis of neutrophils and might be a promising drug for the treatment of particulate matter-induced lung inflammation.
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Usefulness of bevacizumab-induced hypertension in patients with metastatic colorectal cancer: an updated meta-analysis

Chun-Jing Zhang, Shu-Ying Zhang, Chun-Di Zhang, Chun-Rong Lin, Xue-Yan Li, Qiu-Yan Li, Hai-Tao Yu,

https://doi.org/10.18632/aging.101478 pp 1424—1441

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Zhang C, Zhang S, Zhang C, Lin C, Li X, Li Q, Yu H, . Usefulness of bevacizumab-induced hypertension in patients with metastatic colorectal cancer: an updated meta-analysis. Aging (Albany NY). 2018 Jun 2110:1424-1441. https://doi.org/10.18632/aging.101478

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                TY  - JOUR
                AU  - Zhang, Chun-Jing 
                AU  - Zhang, Shu-Ying 
                AU  - Zhang, Chun-Di 
                AU  - Lin, Chun-Rong 
                AU  - Li, Xue-Yan 
                AU  - Li, Qiu-Yan 
                AU  - Yu, Hai-Tao 
                TI  - Usefulness of bevacizumab-induced hypertension in patients with metastatic colorectal cancer: an updated meta-analysis
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101478
                DO  - 10.18632/aging.101478
                SP  - 1424
                EP  - 1441
                PY  - 
                AB  - We tested the hypothesis that bevacizumab-induced hypertension may be a useful predictor for objective response rate, progression-free and overall survival in patients with metastatic colorectal cancer via a comprehensive meta-analysis. Search process, article selection and data extraction were independently performed by two investigators. Statistical analyses were conducted using the STATA/SE software. Fourteen independent studies and 2292 study subjects were synthesized. Overall relative risk of objective response rate for bevacizumab-induced hypertension was 2.03 (95% confidence interval [CI]: 1.18-3.48, p=0.01), with significant heterogeneity and publication bias, whereas unbiased estimate was nonsignificant after considering potentially missing studies. Overall hazard ratio for progression-free survival was 0.58 (95% CI: 0.43-0.77, p&lt;0.001), with significant heterogeneity and publication bias, and unbiased estimate was significant (hazard ratio: 0.52, 95% CI: 0.41-0.66, p&lt;0.001). Overall hazard ratio for overall survival was 0.51 (95% CI: 0.39-0.65, p&lt;0.001), and this estimate was not likely confounded by heterogeneity or publication bias. Subgroup and meta-regression analyses suggested that hypertension grade of controls, sample size, age and gender were possible causes of heterogeneity. Taken together, our findings indicate that bevacizumab-induced hypertension can predict progress-free survival and overall survival in patients with metastatic colorectal cancer, whereas its prediction for objective response rate was nonsignificant.
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Secreted α-Klotho maintains cartilage tissue homeostasis by repressing NOS2 and ZIP8-MMP13 catabolic axis

Paul Chuchana, Anne-Laure Mausset-Bonnefont, Marc Mathieu, Francisco Espinoza, Marisa Teigell, Karine Toupet, Chantal Ripoll, Farida Djouad, Danièle Noel, Christian Jorgensen, Jean-Marc Brondello,

https://doi.org/10.18632/aging.101481 pp 1442—1453

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Chuchana P, Mausset-Bonnefont A, Mathieu M, Espinoza F, Teigell M, Toupet K, Ripoll C, Djouad F, Noel D, Jorgensen C, Brondello J, . Secreted α-Klotho maintains cartilage tissue homeostasis by repressing NOS2 and ZIP8-MMP13 catabolic axis. Aging (Albany NY). 2018 Jun 1910:1442-1453. https://doi.org/10.18632/aging.101481

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 TY - JOUR
 AU - Chuchana, Paul 
 AU - Mausset-Bonnefont, Anne-Laure 
 AU - Mathieu, Marc 
 AU - Espinoza, Francisco 
 AU - Teigell, Marisa 
 AU - Toupet, Karine 
 AU - Ripoll, Chantal 
 AU - Djouad, Farida 
 AU - Noel, Danièle 
 AU - Jorgensen, Christian 
 AU - Brondello, Jean-Marc 
 TI - Secreted α-Klotho maintains cartilage tissue homeostasis by repressing NOS2 and ZIP8-MMP13 catabolic axis
 JO - 
 JA - Aging (Albany NY)
 VL - 10
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101481
 DO - 10.18632/aging.101481
 SP - 1442
 EP - 1453
 PY - 
 AB - Progressive loss of tissue homeostasis is a hallmark of numerous age-related pathologies, including osteoarthritis (OA). Accumulation of senescent chondrocytes in joints contributes to the age-dependent cartilage loss of functions through the production of hypertrophy-associated catabolic matrix-remodeling enzymes and pro-inflammatory cytokines. Here, we evaluated the effects of the secreted variant of the anti-aging hormone α-Klotho on cartilage homeostasis during both cartilage formation and OA development. First, we found that α-Klotho expression was detected during mouse limb development, and transiently expressed during in vitro chondrogenic differentiation of bone marrow-derived mesenchymal stem cells. Genome-wide gene array analysis of chondrocytes from OA patients revealed that incubation with recombinant secreted α-Klotho repressed expression of the NOS2 and ZIP8/MMP13 catabolic remodeling axis. Accordingly, α-Klotho expression was reduced in chronically IL1β-treated chondrocytes and in cartilage of an OA mouse model. Finally, in vivo intra-articular secreted α-Kotho gene transfer delays cartilage degradation in the OA mouse model. Altogether, our results reveal a new tissue homeostatic function for this anti-aging hormone in protecting against OA onset and progression.
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Naked mole rat cells display more efficient excision repair than mouse cells

Alexei Evdokimov, Mikhail Kutuzov, Irina Petruseva, Natalia Lukjanchikova, Elena Kashina, Ekaterina Kolova, Tatyana Zemerova, Svetlana Romanenko, Polina Perelman, Dmitry Prokopov, Andrei Seluanov, Vera Gorbunova, Alexander Graphodatsky, Vladimir Trifonov, Svetlana Khodyreva, Olga Lavrik,

https://doi.org/10.18632/aging.101482 pp 1454—1473

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Evdokimov A, Kutuzov M, Petruseva I, Lukjanchikova N, Kashina E, Kolova E, Zemerova T, Romanenko S, Perelman P, Prokopov D, Seluanov A, Gorbunova V, Graphodatsky A, et al, . Naked mole rat cells display more efficient excision repair than mouse cells. Aging (Albany NY). 2018 Jun 2010:1454-1473. https://doi.org/10.18632/aging.101482

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                TY  - JOUR
                AU  - Evdokimov, Alexei 
                AU  - Kutuzov, Mikhail 
                AU  - Petruseva, Irina 
                AU  - Lukjanchikova, Natalia 
                AU  - Kashina, Elena 
                AU  - Kolova, Ekaterina 
                AU  - Zemerova, Tatyana 
                AU  - Romanenko, Svetlana 
                AU  - Perelman, Polina 
                AU  - Prokopov, Dmitry 
                AU  - Seluanov, Andrei 
                AU  - Gorbunova, Vera 
                AU  - Graphodatsky, Alexander 
                AU  - Trifonov, Vladimir 
                AU  - Khodyreva, Svetlana 
                AU  - Lavrik, Olga 
                TI  - Naked mole rat cells display more efficient excision repair than mouse cells
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101482
                DO  - 10.18632/aging.101482
                SP  - 1454
                EP  - 1473
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Evdokimov, Alexei 
                AU  - Kutuzov, Mikhail 
                AU  - Petruseva, Irina 
                AU  - Lukjanchikova, Natalia 
                AU  - Kashina, Elena 
                AU  - Kolova, Ekaterina 
                AU  - Zemerova, Tatyana 
                AU  - Romanenko, Svetlana 
                AU  - Perelman, Polina 
                AU  - Prokopov, Dmitry 
                AU  - Seluanov, Andrei 
                AU  - Gorbunova, Vera 
                AU  - Graphodatsky, Alexander 
                AU  - Trifonov, Vladimir 
                AU  - Khodyreva, Svetlana 
                AU  - Lavrik, Olga 
                TI  - Naked mole rat cells display more efficient excision repair than mouse cells
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101482
                DO  - 10.18632/aging.101482
                SP  - 1454
                EP  - 1473
                PY  - 
                AB  - Naked mole rat (NMR) is the long-lived and tumor-resistant rodent. NMRs possess multiple adaptations that may contribute to longevity and cancer-resistance. However, whether NMRs have more efficient DNA repair have not been directly tested. Here we compared base excision repair (BER) and nucleotide excision repair (NER) systems in extracts from NMR and mouse fibroblasts after UVC irradiation. Transcript levels of the key repair enzymes demonstrated in most cases higher inducibility in the mouse vs the NMR cells. Ratios of repair enzymes activities in the extracts somewhat varied depending on post-irradiation time. NMR cell extracts were 2–3-fold more efficient at removing the bulky lesions, 1.5–3-fold more efficient at removing uracil, and about 1.4-fold more efficient at cleaving the AP-site than the mouse cells, while DNA polymerase activities being as a whole higher in the mouse demonstrate different patterns of product distribution. The level of poly(ADP-ribose) synthesis was 1.4–1.8-fold higher in the NMR cells. Furthermore, NMR cell extracts displayed higher binding of PARP1 to DNA probes containing apurinic/apyrimidinic site or photo-reactive DNA lesions. Cumulatively, our results suggest that the NMR has more efficient excision repair systems than the mouse, which may contribute to longevity and cancer resistance of this species.
                ER  -

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microRNA-21 regulates astrocytic reaction post-acute phase of spinal cord injury through modulating TGF-β signaling

Ronghan Liu, Wenzhao Wang, Shuya Wang, Wei Xie, Hongfei Li, Bin Ning,

https://doi.org/10.18632/aging.101484 pp 1474—1488

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Liu R, Wang W, Wang S, Xie W, Li H, Ning B, . microRNA-21 regulates astrocytic reaction post-acute phase of spinal cord injury through modulating TGF-β signaling. Aging (Albany NY). 2018 Jun 2310:1474-1488. https://doi.org/10.18632/aging.101484

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                TY  - JOUR
                AU  - Liu, Ronghan 
                AU  - Wang, Wenzhao 
                AU  - Wang, Shuya 
                AU  - Xie, Wei 
                AU  - Li, Hongfei 
                AU  - Ning, Bin 
                TI  - microRNA-21 regulates astrocytic reaction post-acute phase of spinal cord injury through modulating TGF-β signaling
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101484
                DO  - 10.18632/aging.101484
                SP  - 1474
                EP  - 1488
                PY  - 
                AB  - Astrogliosis following spinal cord injury (SCI) was considered as a negative factor for neural regeneration. We found that miR-21 was significantly upregulated after SCI. So, we aim to determine whether miR-21 acts in a positive manner post SCI. In vitro, we measured the proliferation, apoptosis and cytokine secretion of primary cultured astrocytes after modulating the expression of miR-21 by western blot, RT-PCR and immunofluorescence. In vivo, we performed a modified Allen’s weight drop model. Manipulation of the miR-21 expression level was achieved by interfering with antagomir and agomir. Clinic score was evaluated and recorded every day. Then, western blot, immunohistochemistry, TUNEL assay and ELISA were performed to detect pathological and functional alterations. Our results demonstrate that miR-21 can modulate the secretion, proliferation and apoptosis of astrocytes to promote recovery after SCI both in vivo and in vitro. These effects are likely mediated through transforming growth factor beta mediated targeting of the PI3K/Akt/mTOR pathway. These data suggest that miR-21 can regulate astrocytic function, then promote the functional recovery after SCI. We therefore highlight the positive effects of miR-21 after SCI.
                ER  -

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Regulatory RNA binding proteins contribute to the transcriptome-wide splicing alterations in human cellular senescence

Qiongye Dong, Lei Wei, Michael Q. Zhang, Xiaowo Wang,

https://doi.org/10.18632/aging.101485 pp 1489—1505

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Dong Q, Wei L, Zhang MQ, Wang X, . Regulatory RNA binding proteins contribute to the transcriptome-wide splicing alterations in human cellular senescence. Aging (Albany NY). 2018 Jun 2410:1489-1505. https://doi.org/10.18632/aging.101485

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                TY  - JOUR
                AU  - Dong, Qiongye 
                AU  - Wei, Lei 
                AU  - Zhang, Michael Q. 
                AU  - Wang, Xiaowo 
                TI  - Regulatory RNA binding proteins contribute to the transcriptome-wide splicing alterations in human cellular senescence
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101485
                DO  - 10.18632/aging.101485
                SP  - 1489
                EP  - 1505
                PY  - 
                AB  - Dysregulation of mRNA splicing has been observed in certain cellular senescence process. However, the common splicing alterations on the whole transcriptome shared by various types of senescence are poorly understood. In order to systematically identify senescence-associated transcriptomic changes in genome-wide scale, we collected RNA sequencing datasets of different human cell types with a variety of senescence-inducing methods from public databases and performed meta-analysis. First, we discovered that a group of RNA binding proteins were consistently down-regulated in diverse senescent samples and identified 406 senescence-associated common differential splicing events. Then, eight differentially expressed RNA binding proteins were predicted to regulate these senescence-associated splicing alterations through an enrichment analysis of their RNA binding information, including motif scanning and enhanced cross-linking immunoprecipitation data. In addition, we constructed the splicing regulatory modules that might contribute to senescence-associated biological processes. Finally, it was confirmed that knockdown of the predicted senescence-associated potential splicing regulators through shRNAs in HepG2 cell line could result in senescence-like splicing changes. Taken together, our work demonstrated a broad range of common changes in mRNA splicing switches and detected their central regulatory RNA binding proteins during senescence. These findings would help to better understand the coordinating splicing alterations in cellular senescence.
                ER  -

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Fanconi Anemia complementation group C protein in metabolic disorders

Manoj Nepal, Chi Ma, Guoxiang Xie, Wei Jia, Peiwen Fei,

https://doi.org/10.18632/aging.101487 pp 1506—1522

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Nepal M, Ma C, Xie G, Jia W, Fei P, . Fanconi Anemia complementation group C protein in metabolic disorders. Aging (Albany NY). 2018 Jun 2110:1506-1522. https://doi.org/10.18632/aging.101487

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                TY  - JOUR
                AU  - Nepal, Manoj 
                AU  - Ma, Chi 
                AU  - Xie, Guoxiang 
                AU  - Jia, Wei 
                AU  - Fei, Peiwen 
                TI  - Fanconi Anemia complementation group C protein in metabolic disorders
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101487
                DO  - 10.18632/aging.101487
                SP  - 1506
                EP  - 1522
                PY  - 
                AB  - Given importance of 22-Fanconi Anemia (FA) proteins together to act in a signaling pathway in preventing deleterious clinical symptoms, e.g. severe bone marrow failure, congenital defects, an early onset of aging and cancer, studies on each FA protein become increasingly attractive. However, an unbiased and systematic investigation of cellular effects resulting from each FA protein is missing. Here, we report roles of FA complementation C group protein (FANCC) in the protection from metabolic disorders. This study was prompted by the diabetes-prone feature displayed in FANCC knockout mice, which is not typically shown in patients with FA. We found that in cells expressing FANCC at different levels, there are representative alterations in metabolites associated with aging (glycine, citrulline, ornithine, L-asparagine, L-tyrosine, L-arginine, L-glutamine, L-leucine, L-isoleucine, L-valine, L-proline and L-alanine), Diabetes Mellitus (DM) (carbon monoxide, collagens, fatty acids, D-glucose, fumaric acid, 2-oxoglutaric acid, C3), inflammation (inosine, L-arginine, L-isoleucine, L-leucine, L-lysine, L-phenylalanine, hypoxanthine, L-methionine), and cancer ( L-methionine, sphingomyelin, acetyl-L-carnitine, L-aspartic acid, L-glutamic acid, niacinamide, phospho-rylethanolamine). We also found that FANCC can act in an FA-pathway-independent manner in tumor suppression. Collectively, featured-metabolic alterations are readouts of functional mechanisms underlying reduced tumorigenicity driven by FANCC, demonstrating close links among cancer, aging, inflammation and DM.
                ER  -

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Linc00472 suppresses proliferation and promotes apoptosis through elevating PDCD4 expression by sponging miR-196a in colorectal cancer

Yafei Ye, Shengnan Yang, Yanping Han, Jingjing Sun, Lijuan Xv, Lina Wu, Yongfeng Wang, Liang Ming,

https://doi.org/10.18632/aging.101488 pp 1523—1533

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Ye Y, Yang S, Han Y, Sun J, Xv L, Wu L, Wang Y, Ming L, . Linc00472 suppresses proliferation and promotes apoptosis through elevating PDCD4 expression by sponging miR-196a in colorectal cancer. Aging (Albany NY). 2018 Jun 2110:1523-1533. https://doi.org/10.18632/aging.101488

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                TY  - JOUR
                AU  - Ye, Yafei 
                AU  - Yang, Shengnan 
                AU  - Han, Yanping 
                AU  - Sun, Jingjing 
                AU  - Xv, Lijuan 
                AU  - Wu, Lina 
                AU  - Wang, Yongfeng 
                AU  - Ming, Liang 
                TI  - Linc00472 suppresses proliferation and promotes apoptosis through elevating PDCD4 expression by sponging miR-196a in colorectal cancer
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 10
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101488
                DO  - 10.18632/aging.101488
                SP  - 1523
                EP  - 1533
                PY  - 
                AB  - Long intergenic non-coding RNA Linc00472 has been considered as a tumor suppressor in some cancers. However, the function and mechanism of Linc00472 in colorectal cancer has not been well elucidated. In this study, we found that Linc00472 was down-regulated in colorectal cancer tissues and cells. Elevated Linc00472 expression suppressed proliferation and induced apoptosis in colorectal cancer cells. Moreover, Linc00472 acted as a competing endogenous RNA (ceRNA) of miR-196a to release programmed cell death 4 (PDCD4). Furthermore, miR-196a overexpression or PDCD4 knockdown reversed Linc00472-mediated proliferation inhibition and apoptosis induction in colorectal cancer cells. Ectopic Linc00472 expression hindered tumor growth in vivo. Our study demonstrated that Linc00472 suppressed proliferation and induced apoptosis through up-regulating PDCD4 by decoying miR-196a, which may be an effective therapeutic target for colorectal cancer.
                ER  -

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Volume 10, Issue 6

About the Cover

Editorials

Claus Lamm, Federica Riva, Giorgia Silani,

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Ning Kon, Wei Gu,

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Koen Cuypers, Celine Maes, Stephan P. Swinnen,

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Hongyuan Wang, Zhizhou Zhang, David Gems,

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Marie Kveiborg, Gary Thomas,

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Research Papers

Diangeng Li, Delong Zhao, Weiguang Zhang, Qian Ma, Dong Liu, Qi Huang, Ying Zheng, Xueyuan Bai, Xuefeng Sun, Xiangmei Chen,

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Megan E. Rowland, Yan Jiang, Frank Beier, Nathalie G. Bérubé,

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Su-Jeong Kim, Hemal H. Mehta, Junxiang Wan, Chisaka Kuehnemann, Jingcheng Chen, Ji-Fan Hu, Andrew R. Hoffman, Pinchas Cohen,

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Gaofeng Zhan, Ning Yang, Shan Li, Niannian Huang, Xi Fang, Jie Zhang, Bin Zhu, Ling Yang, Chun Yang, Ailin Luo,

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Andrea Costantini, Nadia Viola, Antonella Berretta, Roberta Galeazzi, Giulia Matacchione, Jacopo Sabbatinelli, Gianluca Storci, Serena De Matteis, Luca Butini, Maria Rita Rippo, Antonio Domenico Procopio, Daniele Caraceni, Roberto Antonicelli, Fabiola Olivieri, Massimiliano Bonafè,

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Qiuling Sang, Xiaoyang Liu, Libo Wang, Ling Qi, Wenping Sun, Weiyao Wang, Yajuan Sun, Haina Zhang,

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Wang Jiashi, Qiu Chuang, Zhang Zhenjun, Wang Guangbin, Li Bin, He Ming,

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Ravirajsinh N. Jadeja, Folami L. Powell, Malita A. Jones, Jasmine Fuller, Ethan Joseph, Menaka C. Thounaojam, Manuela Bartoli, Pamela M. Martin,

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Zhangyong Xia, Mingliang Gu, Xiaodong Jia, Xiaoting Wang, Chunxia Wu, Jiangwen Guo, Liyong Zhang, Yifeng Du, Jiyue Wang,

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Kenneth L. Seldeen, Manhui Pang, Merced M. Leiker, Jonathan E. Bard, Maria Rodríguez-Gonzalez, Mireya Hernandez, Zachary Sheridan, Norma Nowak, Bruce R. Troen,

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Chi Yang, Ying Jiao, Bing Wei, Zeyi Yang, Jin-Fu Wu, Jorgen Jensen, Wei-Horng Jean, Chih-Yang Huang, Chia-Hua Kuo,

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Jin Zhang, Lixiao Yang, Xiaohong Xiang, Zhuoying Li, Kai Qu, Ke Li,

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Chang Luo, Jiawu Zhao, Mei Chen, Heping Xu,

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Qizhi Cao, Shude Yang, Qing Lv, Yan Liu, Li Li, Xiaojie Wu, Guiwu Qu, Xiaoli He, Xiaoshu Zhang, Shuqin Sun, Boqing Li, Jing An, Tao Hu, Jiangnan Xue,