学科主题基础医学
SIRT1 Overexpression Antagonizes Cellular Senescence with Activated ERK/S6k1 Signaling in Human Diploid Fibroblasts
Huang, Jing1,2; Gan, Qini1,2; Han, Limin1,2; Li, Jian1,2; Zhang, Hai1,2; Sun, Ying1,2; Zhang, Zongyu1,2; Tong, Tanjun1,2
刊名PLOS ONE
2008-03-05
DOI10.1371/journal.pone.0001710
3期:3
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
英文摘要

Sir2, a NAD-dependent deacetylase, modulates lifespan in yeasts, worms and flies. The SIRT1, mammalian homologue of Sir2, regulates signaling for favoring survival in stress. But whether SIRT1 has the function to influence cell viability and senescence under non-stressed conditions in human diploid fibroblasts is far from unknown. Our data showed that enforced SIRT1 expression promoted cell proliferation and antagonized cellular senescence with the characteristic features of delayed Senescence-Associated beta-galactosidase (SA-beta-gal) staining, reduced Senescence-Associated Heterochromatic Foci (SAHF) formation and G1 phase arrest, increased cell growth rate and extended cellular lifespan in human fibroblasts, while dominant-negative SIRT1 allele (H363Y) did not significantly affect cell growth and senescence but displayed a bit decreased lifespan.. Western blot results showed that SIRT1 reduced the expression of p16(INK4A) and promoted phosphorylation of Rb. Our data also exposed that overexpression of SIRT1 was accompanied by enhanced activation of ERK and S6K1 signaling. These effects were mimicked in both WI38 cells and 2BS cells by concentration-dependent resveratrol, a SIRT1 activator. It was noted that treatment of SIRT1-.transfected cells with Rapamycin, a mTOR inhibitor, reduced the phosphorylation of S6K1 and the expression of Id1, implying that SIRT1-induced phosphorylation of S6K1 may be partly for the decreased expression of p16(INK4A) and promoted phosphorylation of Rb in 2BS. It was also observed that the expression of SIRT1 and phosphorylation of ERK and S6K1 was declined in senescent 2BS. These findings suggested that SIRT1-promoted cell proliferation and antagonized cellular senescence in human diploid fibroblasts may be, in part, via the activation of ERK/S6K1 signaling.

语种英语
WOS记录号WOS:000260586600006
引用统计
被引频次:101[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/63005
专题北京大学基础医学院_北京大学衰老研究中心
北京大学基础医学院
北京大学临床肿瘤学院_VIP-Ⅱ
作者单位1.Peking Univ, Res Ctr Aging, Beijing 100871, Peoples R China
2.Peking Univ Hlth Sci Ctr, Dept Biochem & Mol Biol, Beijing, Peoples R China
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GB/T 7714
Huang, Jing,Gan, Qini,Han, Limin,et al. SIRT1 Overexpression Antagonizes Cellular Senescence with Activated ERK/S6k1 Signaling in Human Diploid Fibroblasts[J]. PLOS ONE,2008,3(3).
APA Huang, Jing.,Gan, Qini.,Han, Limin.,Li, Jian.,Zhang, Hai.,...&Tong, Tanjun.(2008).SIRT1 Overexpression Antagonizes Cellular Senescence with Activated ERK/S6k1 Signaling in Human Diploid Fibroblasts.PLOS ONE,3(3).
MLA Huang, Jing,et al."SIRT1 Overexpression Antagonizes Cellular Senescence with Activated ERK/S6k1 Signaling in Human Diploid Fibroblasts".PLOS ONE 3.3(2008).
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