Volume 6, Issue 5

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Patel VK, Demontis F, . GDF11/Myostatin and aging. . 6:351-352. https://doi.org/10.18632/aging.100666

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Provider: TY - JOUR AU - Patel, Vishal K. AU - Demontis, Fabio TI - GDF11/Myostatin and aging JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100666 DO - 10.18632/aging.100666 SP - 351 EP - 352 PY - ER -

Provider: TY - JOUR AU - Patel, Vishal K. AU - Demontis, Fabio TI - GDF11/Myostatin and aging JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100666 DO - 10.18632/aging.100666 SP - 351 EP - 352 PY - AB - ER -

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Gal H, Krizhanovsky V, . Cell fusion induced senescence. . 6:353-354. https://doi.org/10.18632/aging.100670

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Provider: TY - JOUR AU - Gal, Hilah AU - Krizhanovsky, Valery TI - Cell fusion induced senescence JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100670 DO - 10.18632/aging.100670 SP - 353 EP - 354 PY - ER -

Provider: TY - JOUR AU - Gal, Hilah AU - Krizhanovsky, Valery TI - Cell fusion induced senescence JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100670 DO - 10.18632/aging.100670 SP - 353 EP - 354 PY - AB - ER -

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Whitaker R, Gil MP, Ding F, Tatar M, Helfand SL, Neretti N, . Dietary switch reveals fast coordinated gene expression changes in Drosophila melanogaster. . 6:355-368. https://doi.org/10.18632/aging.100662

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Provider: TY - JOUR AU - Whitaker, Rachel AU - Gil, M. Pilar AU - Ding, Feifei AU - Tatar, Marc AU - Helfand, Stephen L. AU - Neretti, Nicola TI - Dietary switch reveals fast coordinated gene expression changes in <i>Drosophila melanogaster</i> JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100662 DO - 10.18632/aging.100662 SP - 355 EP - 368 PY - ER -

Provider: TY - JOUR AU - Whitaker, Rachel AU - Gil, M. Pilar AU - Ding, Feifei AU - Tatar, Marc AU - Helfand, Stephen L. AU - Neretti, Nicola TI - Dietary switch reveals fast coordinated gene expression changes in <i>Drosophila melanogaster</i> JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100662 DO - 10.18632/aging.100662 SP - 355 EP - 368 PY - AB - Dietary restriction (DR) reduces age-specific mortality and increases lifespan in many organisms. DR elicits a large number of physiological changes, however many are undoubtedly not related to longevity. Whole-genome gene expression studies have typically revealed hundreds to thousands of differentially expressed genes in response to DR, and a key open question is which subset of genes mediates longevity. Here we performed transcriptional profiling of fruit flies in a closely spaced time series immediately following a switch to the DR regime and identified four patterns of transcriptional dynamics. Most informatively we find 144 genes rapidly switched to the same level observed in the DR cohort and are hence strong candidates as proximal mediators of reduced mortality upon DR. This class was enriched for genes involved in carbohydrate and fatty acid metabolism. Folate biosynthesis was the only pathway enriched for gene up-regulated upon DR. Four among the down-regulated genes are involved in key regulatory steps within the pentose phosphate pathway, which has been previously associated with lifespan extension in Drosophila. Combined analysis of dietary switch with whole-genome time-course profiling can identify transcriptional responses that are closely associated with and perhaps causal to longevity assurance conferred by dietary restriction. ER -

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Xiong Y, Fru MF, Yu Y, Montani J, Ming X, Yang Z, . Long term exposure to L-arginine accelerates endothelial cell senescence through arginase-II and S6K1 signaling. . 6:369-379. https://doi.org/10.18632/aging.100663

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Provider: TY - JOUR AU - Xiong, Yuyani AU - Fru, Michael Forbiteh AU - Yu, Yi AU - Montani, Jean-Pierre AU - Ming, Xiu-Fen AU - Yang, Zhihong TI - Long term exposure to L-arginine accelerates endothelial cell senescence through arginase-II and S6K1 signaling JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100663 DO - 10.18632/aging.100663 SP - 369 EP - 379 PY - ER -

Provider: TY - JOUR AU - Xiong, Yuyani AU - Fru, Michael Forbiteh AU - Yu, Yi AU - Montani, Jean-Pierre AU - Ming, Xiu-Fen AU - Yang, Zhihong TI - Long term exposure to L-arginine accelerates endothelial cell senescence through arginase-II and S6K1 signaling JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100663 DO - 10.18632/aging.100663 SP - 369 EP - 379 PY - AB - L-arginine supplementation is proposed to improve health status or as adjunct therapy for diseases including cardiovascular diseases. However, controversial results and even detrimental effects of L-arginine supplementation are reported. We investigate potential mechanisms of L-arginine-induced detrimental effects on vascular endothelial cells. Human endothelial cells were exposed to a physiological (0.1 mmol/L) or pharmacological (0.5 mmol/L) concentration of L-arginine for 30 minutes (acute) or 7 days (chronic). The effects of L-arginine supplementation on endothelial senescence phenotype, i.e., levels of senescence-associated beta-galactosidase, expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1, eNOS-uncoupling, arginase-II expression/activity, and mTORC1-S6K1 activity were analyzed. While acute L-arginine treatment enhances endothelial NO production accompanied with superoxide production and activation of S6K1 but no up-regulation of arginase-II, chronic L-arginine supplementation causes endothelial senescence, up-regulation of the adhesion molecule expression, and eNOS-uncoupling (decreased NO and enhanced superoxide production), which are associated with S6K1 activation and up-regulation of arginase-II. Silencing either S6K1 or arginase-II inhibits up-regulation/activation of each other, prevents endothelial dysfunction, adhesion molecule expression, and senescence under the chronic L-arginine supplementation condition. These results demonstrate that S6K1 and arginase-II form a positive circuit mediating the detrimental effects of chronic L-arginine supplementation on endothelial cells. ER -

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Chen S, Yeh F, Lin J, Matsuguchi T, Blackburn E, Lee ET, Howard BV, Zhao J, . Short leukocyte telomere length is associated with obesity in American Indians: The strong heart family study. . 6:380-389. https://doi.org/10.18632/aging.100664

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Provider: TY - JOUR AU - Chen, Shufeng AU - Yeh, Fawn AU - Lin, Jue AU - Matsuguchi, Tet AU - Blackburn, Elizabeth AU - Lee, Elisa T. AU - Howard, Barbara V. AU - Zhao, Jinying TI - Short leukocyte telomere length is associated with obesity in American Indians: The strong heart family study JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100664 DO - 10.18632/aging.100664 SP - 380 EP - 389 PY - ER -

Provider: TY - JOUR AU - Chen, Shufeng AU - Yeh, Fawn AU - Lin, Jue AU - Matsuguchi, Tet AU - Blackburn, Elizabeth AU - Lee, Elisa T. AU - Howard, Barbara V. AU - Zhao, Jinying TI - Short leukocyte telomere length is associated with obesity in American Indians: The strong heart family study JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100664 DO - 10.18632/aging.100664 SP - 380 EP - 389 PY - AB - Shorter leukocyte telomere length (LTL) has been associated with a wide range of age-related disorders including cardiovascular disease (CVD) and diabetes. Obesity is an important risk factor for CVD and diabetes. The association of LTL with obesity is not well understood. This study for the first time examines the association of LTL with obesity indices including body mass index, waist circumference, percent body fat, waist-to-hip ratio, and waist-to-height ratio in 3,256 American Indians (14-93 years old, 60% women) participating in the Strong Heart Family Study. Association of LTL with each adiposity index was examined using multivariate generalized linear mixed model, adjusting for chronological age, sex, study center, education, lifestyle (smoking, alcohol consumption, and total energy intake), high-sensitivity C-reactive protein, hypertension and diabetes. Results show that obese participants had significantly shorter LTL than non-obese individuals (age-adjusted P=0.0002). Multivariate analyses demonstrate that LTL was significantly and inversely associated with all of the studied obesity parameters. Our results may shed light on the potential role of biological aging in pathogenesis of obesity and its comorbidities. ER -

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Emran S, Yang M, He X, Zandveld J, Piper MDW, . Target of rapamycin signalling mediates the lifespan-extending effects of dietary restriction by essential amino acid alteration. . 6:390-398. https://doi.org/10.18632/aging.100665

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Provider: TY - JOUR AU - Emran, Sahar AU - Yang, Mingyao AU - He, Xiaoli AU - Zandveld, Jelle AU - Piper, Matthew D. W. TI - Target of rapamycin signalling mediates the lifespan-extending effects of dietary restriction by essential amino acid alteration JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100665 DO - 10.18632/aging.100665 SP - 390 EP - 398 PY - ER -

Provider: TY - JOUR AU - Emran, Sahar AU - Yang, Mingyao AU - He, Xiaoli AU - Zandveld, Jelle AU - Piper, Matthew D. W. TI - Target of rapamycin signalling mediates the lifespan-extending effects of dietary restriction by essential amino acid alteration JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100665 DO - 10.18632/aging.100665 SP - 390 EP - 398 PY - AB - Dietary restriction (DR), defined as a moderate reduction in food intake short of malnutrition, has been shown to extend healthy lifespan in a diverse range of organisms, from yeast to primates. Reduced signalling through the insulin/IGF-like (IIS) and Target of Rapamycin (TOR) signalling pathways also extend lifespan. In Drosophila melanogaster the lifespan benefits of DR can be reproduced by modulating only the essential amino acids in yeast based food. Here, we show that pharmacological downregulation of TOR signalling, but not reduced IIS, modulates the lifespan response to DR by amino acid alteration. Of the physiological responses flies exhibit upon DR, only increased body fat and decreased heat stress resistance phenotypes correlated with longevity via reduced TOR signalling. These data indicate that lowered dietary amino acids promote longevity via TOR, not by enhanced resistance to molecular damage, but through modified physiological conditions that favour fat accumulation. ER -

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Pinto AR, Godwin JW, Chandran A, Hersey L, Ilinykh A, Debuque R, Wang L, Rosenthal NA, . Age-related changes in tissue macrophages precede cardiac functional impairment. . 6:399-413. https://doi.org/10.18632/aging.100669

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Provider: TY - JOUR AU - Pinto, Alexander R. AU - Godwin, James W. AU - Chandran, Anjana AU - Hersey, Lucy AU - Ilinykh, Alexei AU - Debuque, Ryan AU - Wang, Lina AU - Rosenthal, Nadia A. TI - Age-related changes in tissue macrophages precede cardiac functional impairment JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100669 DO - 10.18632/aging.100669 SP - 399 EP - 413 PY - ER -

Provider: TY - JOUR AU - Pinto, Alexander R. AU - Godwin, James W. AU - Chandran, Anjana AU - Hersey, Lucy AU - Ilinykh, Alexei AU - Debuque, Ryan AU - Wang, Lina AU - Rosenthal, Nadia A. TI - Age-related changes in tissue macrophages precede cardiac functional impairment JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100669 DO - 10.18632/aging.100669 SP - 399 EP - 413 PY - AB - Cardiac tissue macrophages (cTMs) are abundant in the murine heart but the extent to which the cTM phenotype changes with age is unknown. This study characterizes aging-dependent phenotypic changes in cTM subsets. Using the Cx3cr1GFP/+ mouse reporter line where GFP marks cTMs, and the tissue macrophage marker Mrc1, we show that two major cardiac tissue macrophage subsets, Mrc1−GFPhi and Mrc1+GFPhi cTMs, are present in the young (&lt;10 week old) mouse heart, and a third subset, Mrc1+GFPlo, comprises ~50% of total Mrc1+ cTMs from 30 weeks of age. Immunostaining and functional assays show that Mrc1+ cTMs are the principal myeloid sentinels in the mouse heart and that they retain proliferative capacity throughout life. Gene expression profiles of the two Mrc1+ subsets also reveal that Mrc1+GFPlo cTMs have a decreased number of immune response genes (Cx3cr1, Lpar6, CD9, Cxcr4, Itga6 and Tgfβr1), and an increased number of fibrogenic genes (Ltc4s, Retnla, Fgfr1, Mmp9 and Ccl24), consistent with a potential role for cTMs in cardiac fibrosis. These findings identify early age-dependent gene expression changes in cTMs, with significant implications for cardiac tissue injury responses and aging-associated cardiac fibrosis. ER -

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Chen S, Lin J, Matsuguchi T, Blackburn E, Yeh F, Best LG, Devereux RB, Lee ET, Howard BV, Roman MJ, Zhao J, . Short leukocyte telomere length predicts incidence and progression of carotid atherosclerosis in American Indians: The Strong Heart Family Study. . 6:414-427. https://doi.org/10.18632/aging.100671

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Provider: TY - JOUR AU - Chen, Shufeng AU - Lin, Jue AU - Matsuguchi, Tet AU - Blackburn, Elizabeth AU - Yeh, Fawn AU - Best, Lyle G. AU - Devereux, Richard B. AU - Lee, Elisa T. AU - Howard, Barbara V. AU - Roman, Mary J. AU - Zhao, Jinying TI - Short leukocyte telomere length predicts incidence and progression of carotid atherosclerosis in American Indians: The Strong Heart Family Study JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100671 DO - 10.18632/aging.100671 SP - 414 EP - 427 PY - ER -

Provider: TY - JOUR AU - Chen, Shufeng AU - Lin, Jue AU - Matsuguchi, Tet AU - Blackburn, Elizabeth AU - Yeh, Fawn AU - Best, Lyle G. AU - Devereux, Richard B. AU - Lee, Elisa T. AU - Howard, Barbara V. AU - Roman, Mary J. AU - Zhao, Jinying TI - Short leukocyte telomere length predicts incidence and progression of carotid atherosclerosis in American Indians: The Strong Heart Family Study JO - JA - VL - 6 IS - 5 PB - SN - UR - https://doi.org/10.18632/aging.100671 DO - 10.18632/aging.100671 SP - 414 EP - 427 PY - AB - Short leukocyte telomere length (LTL) has been associated with atherosclerosis in cross-sectional studies, but the prospective relationship between telomere shortening and risk of developing carotid atherosclerosis has not been well-established. This study examines whether LTL at baseline predicts incidence and progression of carotid atherosclerosis in American Indians in the Strong Heart Study. The analysis included 2,819 participants who were free of overt cardiovascular disease at baseline (2001-2003) and were followed through the end of 2006-2009 (average 5.5-yr follow-up). Discrete atherosclerotic plaque was defined as focal protrusion with an arterial wall thickness ≥50% the surrounding wall. Carotid progression was defined as having a higher plaque score at the end of study follow-up compared to baseline. Associations of LTL with incidence and progression of carotid plaque were examined using Cox proportional hazard regression, adjusting for standard coronary risk factors. Compared to participants in the highest LTL tertile, those in the lowest tertile had significantly elevated risk for both incident plaque (HR, 1.49; 95% CI, 1.09–2.03) and plaque progression (HR, 1.61; 95% CI, 1.26–2.07). Our results provide initial evidence for a potential prognostic utility of LTL in risk prediction for atherosclerosis. ER -

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