Volume 5, Issue 2

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Liu B, Zhou Z, . Activation of SIRT1 by Resveratrol requires lamin A. . 5:94-95. https://doi.org/10.18632/aging.100532

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Provider: TY - JOUR AU - Liu, Baohua AU - Zhou, Zhongjun TI - Activation of SIRT1 by Resveratrol requires lamin A JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100532 DO - 10.18632/aging.100532 SP - 94 EP - 95 PY - ER -

Provider: TY - JOUR AU - Liu, Baohua AU - Zhou, Zhongjun TI - Activation of SIRT1 by Resveratrol requires lamin A JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100532 DO - 10.18632/aging.100532 SP - 94 EP - 95 PY - AB - ER -

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Rajagopalan S, Long EO, . A positive role for senescence in reproduction?. . 5:96-97. https://doi.org/10.18632/aging.100538

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Provider: TY - JOUR AU - Rajagopalan, Sumati AU - Long, Eric O. TI - A positive role for senescence in reproduction? JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100538 DO - 10.18632/aging.100538 SP - 96 EP - 97 PY - ER -

Provider: TY - JOUR AU - Rajagopalan, Sumati AU - Long, Eric O. TI - A positive role for senescence in reproduction? JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100538 DO - 10.18632/aging.100538 SP - 96 EP - 97 PY - AB - ER -

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Tran S, Rizos H, . Human nevi lack distinguishing senescence traits. . 5:98-99. https://doi.org/10.18632/aging.100537

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Provider: TY - JOUR AU - Tran, Sieu AU - Rizos, Helen TI - Human nevi lack distinguishing senescence traits JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100537 DO - 10.18632/aging.100537 SP - 98 EP - 99 PY - ER -

Provider: TY - JOUR AU - Tran, Sieu AU - Rizos, Helen TI - Human nevi lack distinguishing senescence traits JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100537 DO - 10.18632/aging.100537 SP - 98 EP - 99 PY - AB - ER -

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Livi CB, Hardman RL, Christy BA, Dodds SG, Jones D, Williams C, Strong R, Bokov A, Javors MA, Ikeno Y, Hubbard G, Hasty P, Sharp ZD, . Rapamycin extends life span of Rb1^+/− mice by inhibiting neuroendocrine tumors. . 5:100-110. https://doi.org/10.18632/aging.100533

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Provider: TY - JOUR AU - Livi, Carolina B. AU - Hardman, Rulon L. AU - Christy, Barbara A. AU - Dodds, Sherry G. AU - Jones, Diane AU - Williams, Charnae AU - Strong, Randy AU - Bokov, Alex AU - Javors, Martin A. AU - Ikeno, Yuji AU - Hubbard, Gene AU - Hasty, Paul AU - Sharp, Zelton Dave TI - Rapamycin extends life span of Rb1^+/− mice by inhibiting neuroendocrine tumors JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100533 DO - 10.18632/aging.100533 SP - 100 EP - 110 PY - ER -

Provider: TY - JOUR AU - Livi, Carolina B. AU - Hardman, Rulon L. AU - Christy, Barbara A. AU - Dodds, Sherry G. AU - Jones, Diane AU - Williams, Charnae AU - Strong, Randy AU - Bokov, Alex AU - Javors, Martin A. AU - Ikeno, Yuji AU - Hubbard, Gene AU - Hasty, Paul AU - Sharp, Zelton Dave TI - Rapamycin extends life span of Rb1^+/− mice by inhibiting neuroendocrine tumors JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100533 DO - 10.18632/aging.100533 SP - 100 EP - 110 PY - AB - Chronic treatment of mice with an enterically released formulation of rapamycin (eRapa) extends median and maximum life span, partly by attenuating cancer. The mechanistic basis of this response is not known. To gain a better understanding of these in vivo effects, we used a defined preclinical model of neuroendocrine cancer, Rb1+/− mice. Previous results showed that diet restriction (DR) had minimal or no effect on the lifespan of Rb1+/− mice, suggesting that the beneficial response to DR is dependent on pRb1. Since long-term eRapa treatment may at least partially mimic chronic DR in lifespan extension, we predicted that it would have a minimal effect in Rb1+/− mice. Beginning at 9 weeks of age until death, we fed Rb1+/− mice a diet without or with eRapa at 14 mg/kg food, which results in an approximate dose of 2.24 mg/kg body weight per day, and yielded rapamycin blood levels of about 4 ng/ml. Surprisingly, we found that eRapa dramatically extended life span of both female and male Rb1+/− mice, and slowed the appearance and growth of pituitary and decreased the incidence of thyroid tumors commonly observed in these mice. In this model, eRapa appears to act differently than DR, suggesting diverse mechanisms of action on survival and anti-tumor effects. In particular the beneficial effects of rapamycin did not depend on the dose of Rb1. ER -

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Liu Y, Huang Y, Wang Z, Huang Y, Li X, Louie A, Wei G, Mao J, . Temporal mTOR inhibition protects Fbxw7-deficient mice from radiation-induced tumor development. . 5:111-119. https://doi.org/10.18632/aging.100535

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Provider: TY - JOUR AU - Liu, Yueyong AU - Huang, Yurong AU - Wang, Zeran AU - Huang, Yong AU - Li, Xiaohua AU - Louie, Alexander AU - Wei, Guangwei AU - Mao, Jian-Hua TI - Temporal mTOR inhibition protects Fbxw7-deficient mice from radiation-induced tumor development JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100535 DO - 10.18632/aging.100535 SP - 111 EP - 119 PY - ER -

Provider: TY - JOUR AU - Liu, Yueyong AU - Huang, Yurong AU - Wang, Zeran AU - Huang, Yong AU - Li, Xiaohua AU - Louie, Alexander AU - Wei, Guangwei AU - Mao, Jian-Hua TI - Temporal mTOR inhibition protects Fbxw7-deficient mice from radiation-induced tumor development JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100535 DO - 10.18632/aging.100535 SP - 111 EP - 119 PY - AB - FBXW7 acts as a tumor suppressor in numerous types of human cancers through ubiquitination of different oncoproteins including mTOR. However, how the mutation/loss of Fbxw7 results in tumor development remains largely unknown. Here we report that downregulation of mTOR by radiation is Fbxw7-dependent, and short-term mTOR inhibition by rapamycin after exposure to radiation significantly postpones tumor development in Fbxw7/p53 double heterozygous (Fbxw7+/−p53+/−) mice but not in p53 single heterozygous (p53+/−) mice. Tumor latency of rapamycin treated Fbxw7+/−p53+/− mice is remarkably similar to those of p53+/− mice while placebo treated Fbxw7+/−p53+/− mice develop tumor significantly earlier than placebo treated p53+/− mice. Furthermore, we surprisingly find that, although temporal treatment of rapamycin is given at a young age, the inhibition of mTOR activity sustainably remains in tumors. These results indicate that inhibition of mTOR signaling pathway suppresses the contribution of Fbxw7 loss toward tumor development. ER -

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Jeyapalan JC, Sedivy JM, . How to measure RNA expression in rare senescent cells expressing any specific protein such as p16^Ink4a. . 5:120-129. https://doi.org/10.18632/aging.100536

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Provider: TY - JOUR AU - Jeyapalan, Jessie C. AU - Sedivy, John M. TI - How to measure RNA expression in rare senescent cells expressing any specific protein such as p16^Ink4a JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100536 DO - 10.18632/aging.100536 SP - 120 EP - 129 PY - ER -

Provider: TY - JOUR AU - Jeyapalan, Jessie C. AU - Sedivy, John M. TI - How to measure RNA expression in rare senescent cells expressing any specific protein such as p16^Ink4a JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100536 DO - 10.18632/aging.100536 SP - 120 EP - 129 PY - AB - Here we describe a carefully optimized method for the preparation of high quality RNA by flow sorting of formaldehyde fixed senescent cells immunostained for any intracellular antigen. Replicative cellular senescence is a phenomenon of irreversible growth arrest triggered by the accumulation of a discrete number of cell divisions. The underlying cause of senescence due to replicative exhaustion is telomere shortening. We document here a spontaneous and apparently stochastic process that continuously generates senescent cells in cultures fully immortalized with telomerase. In the course of studying this phenomenon we developed a preparative fluorescence activated flow sorting method based on immunofluorescent staining of intracellular antigens that can also deliver RNA suitable for quantitative analysis of global gene expression. The protocols were developed using normal human diploid fibroblasts (HDF) and up to 5×107 cells could be conveniently processed in a single experiment. The methodology is based on formaldehyde crosslinking of cells, followed by permeabilization, antibody staining, flow sorting, reversal of the crosslinks, and recovery of the RNA. We explored key parameters such as crosslink reversal that affect the fragmentation of RNA. The recovered RNA is of high quality for downstream molecular applications based on short range sequence analysis, such qPCR, hybridization microarrays, and next generation sequencing. The RNA was analyzed by Affymetrix Gene Chip expression profiling and compared to RNA prepared by the direct lysis of cells. The correlation between the data sets was very high, indicating that the procedure does not introduce systematic changes in the mRNA transcriptome. The methods presented in this communication should be of interest to many investigators working in diverse model systems. ER -

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Dhahbi JM, Spindler SR, Atamna H, Yamakawa A, Guerrero N, Boffelli D, Mote P, Martin DI, . Deep sequencing identifies circulating mouse miRNAs that are functionally implicated in manifestations of aging and responsive to calorie restriction. . 5:130-141. https://doi.org/10.18632/aging.100540

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Provider: TY - JOUR AU - Dhahbi, Joseph M AU - Spindler, Stephen R AU - Atamna, Hani AU - Yamakawa, Amy AU - Guerrero, Noel AU - Boffelli, Dario AU - Mote, Patricia AU - Martin, David IK TI - Deep sequencing identifies circulating mouse miRNAs that are functionally implicated in manifestations of aging and responsive to calorie restriction JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100540 DO - 10.18632/aging.100540 SP - 130 EP - 141 PY - ER -

Provider: TY - JOUR AU - Dhahbi, Joseph M AU - Spindler, Stephen R AU - Atamna, Hani AU - Yamakawa, Amy AU - Guerrero, Noel AU - Boffelli, Dario AU - Mote, Patricia AU - Martin, David IK TI - Deep sequencing identifies circulating mouse miRNAs that are functionally implicated in manifestations of aging and responsive to calorie restriction JO - JA - VL - 5 IS - 2 PB - SN - UR - https://doi.org/10.18632/aging.100540 DO - 10.18632/aging.100540 SP - 130 EP - 141 PY - AB - MicroRNAs (miRNAs) function to modulate gene expression, and through this property they regulate a broad spectrum of cellular processes. They can circulate in blood and thereby mediate cell-to-cell communication. Aging involves changes in many cellular processes that are potentially regulated by miRNAs, and some evidence has implicated circulating miRNAs in the aging process. In order to initiate a comprehensive assessment of the role of circulating miRNAs in aging, we have used deep sequencing to characterize circulating miRNAs in the serum of young mice, old mice, and old mice maintained on calorie restriction (CR). Deep sequencing identifies a set of novel miRNAs, and also accurately measures all known miRNAs present in serum. This analysis demonstrates that the levels of many miRNAs circulating in the mouse are increased with age, and that the increases can be antagonized by CR. The genes targeted by this set of age-modulated miRNAs are predicted to regulate biological processes directly relevant to the manifestations of aging including metabolic changes, and the miRNAs themselves have been linked to diseases associated with old age. This finding implicates circulating miRNAs in the aging process, raising questions about their tissues of origin, their cellular targets, and their functional role in metabolic changes that occur with aging. ER -

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