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本帖最后由 hnsdlgl 于 2011-11-11 22:13 编辑
) I& Y+ k) E, i- k( \" {naturalkillerce 发表于 2011-11-5 09:32 
( A2 d; C# z" Z0 J& w5 b: \+ Y回复 干细胞换包包 的帖子
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全文已有解释啊，这是因为干细胞(文中的干细胞都是成体干细胞，如间充质干细胞 ...
3 g, q# C$ c8 r/ b又有新进展了，2011年11月10日Nature《清除含衰老标记物p16(Ink4a)的细胞，延缓衰老》
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Nature 479 (7372) | doi:10.1038/nature106001 W& k0 w/ v1 K( F
发表日期：11年11月10日7 P! Z* s( X! {: q1 R# K) l# p5 Y
衰老细胞随年龄增长在组织中积累，但它们实际上是否会引起与年龄相关的功能丧失、或它们的清除是否有好处都不知道。Baker等人利用携带一个名为INK-ATTAC的转基因（该转基因允许通过可诱导的方式将携带衰老生物标记p16Ink4a的细胞清除）的小鼠模型所做研究表明，终身清除衰老细胞，能够延迟与年龄相关的表现型的最初出现时间。而且，晚年的清除会延缓已经出现的与年龄相关的病症的发展。这表明，衰老细胞的确能引起与年龄相关的表现型，而且它们的清除能够防止或延迟与年龄相关的组织功能丧失。$ Y: M( x1 a: ~- b6 B' p
0 L5 G: L0 z( \5 g# l4 UBaker, D. J., T. Wijshake, et al. (2011). "Clearance of p16(Ink4a)-positive senescent cells delays ageing-associated disorders." Nature 479(7372): 232-236.
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5 u% @* ]( x. Z9 X. P5 L6 NAdvanced age is the main risk factor for most chronic diseases and functional deficits in humans, but the fundamental mechanisms that drive ageing remain largely unknown, impeding the development of interventions that might delay or prevent age-related disorders and maximize healthy lifespan. Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cells. Senescent cells accumulate in various tissues and organs with ageing and have been hypothesized to disrupt tissue structure and function because of the components they secrete. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16(Ink4a), to design a novel transgene, INK-ATTAC, for inducible elimination of p16(Ink4a)-positive senescent cells upon administration of a drug. Here we show that in the BubR1 progeroid mouse background, INK-ATTAC removes p16(Ink4a)-positive senescent cells upon drug treatment. In tissues-such as adipose tissue, skeletal muscle and eye-in which p16(Ink4a) contributes to the acquisition of age-related pathologies, life-long removal of p16(Ink4a)-expressing cells delayed onset of these phenotypes. Furthermore, late-life clearance attenuated progression of already established age-related disorders. These data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.
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v( H: i2 W/ R% n* D p: y ?原文请见下面附件 |
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发表于 2011-11-5 15:06
发表于 2011-11-5 17:49
