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神奇的P21,关闭这种基因,人体将可自愈并修复断肢、背伤甚至脑损伤进化的损失两栖动物能再生,但其他动物却在进化过程中失去了该能力断肢、背伤甚至脑损伤的自行修复在未来将成为现实。因为科学家日前发现了一种基因,该基因对这种近乎神奇的能力起关键作用。
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" f, c: B* w% n$ Y9 ]1 ~& @/ n9 `" ~科学家发现p21基因阻碍了人体的自愈能力,而这种能力在包括两栖动物在内的一些生物身上得以延续,但其他动物却在进化过程中失去了该能力。- w# c% z' D, C) m
4 J6 j) Y+ h, U1 N/ R% H关闭p21开启再生
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来自费城维斯拓研究所的科研人员发现缺乏p21的老鼠获得了再生其受损或缺失组织的能力。与其他通过伤疤进行愈合的典型哺乳动物不同,这些老鼠通过形成一种胚基来帮助细胞快速生长。
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6 Z, R) G8 |1 I1 v研究人员发现,p21的缺失导致这些老鼠的细胞活动更类似于胚胎干细胞而非成年哺乳动物细胞。这意味着它们将再生而非修复其躯体。该发现发表于《国家科学院学报》PNAS上,为组织再生与细胞分裂控制的关联提供了确凿的证据。
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科学家们在耳部受损的老鼠身上关闭了p21基因,之后这些老鼠的耳朵再生了。
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任何治疗都可起效8 Q$ `+ w7 f3 C& E# l
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首席科学家艾伦·赫博·卡茨教授指出,“就像断肢的蝾螈一样,这些老鼠将会用健康的组织来取代那些受损甚至缺失的组织,而且不会留下任何伤疤。”1 E$ _& c' `/ |! H3 a1 t
5 {6 Q+ y/ s3 e- M1 @" D“总有一天我们可以通过暂时失活p21以提高人体的再生能力。我们认为任何未来疗法都需要在治疗过程中暂时关闭受伤位置上的p21。这可能需要局部起效药物才能达成。而这将会把副作用降到最低。”(生物谷Bioon.com)
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' N# p& b4 F) C3 G# q' X* X原文:
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, P* f9 i1 s6 s3 ^' |2 |Lack of p21 expression links cell cycle control and appendage regeneration in mice& _, {, G( D5 }
Khamilia Bedelbaevaa,1, Andrew Snydera,1,2, Dmitri Gourevitcha, Lise Clarka, Xiang-Ming Zhanga, John Leferovicha, James M. Cheverudb, Paul Liebermana, and Ellen Heber-Katza,3
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Animals capable of regenerating multiple tissue types, organs, and appendages after injury are common yet sporadic and include some sponge, hydra, planarian, and salamander (i.e., newt and axolotl) species, but notably such regenerative capacity is rare in mammals. The adult MRL mouse strain is a rare exception to the rule that mammals do not regenerate appendage tissue. Certain commonalities, such as blastema formation and basement membrane breakdown at the wound site, suggest that MRL mice may share other features with classical regenerators. As reported here, MRL fibroblast-like cells have a distinct cell-cycle (G2/M accumulation) phenotype and a heightened basal and wound site DNA damage/repair response that is also common to classical regenerators and mammalian embryonic stem cells. Additionally, a neutral and alkaline comet assay displayed a persistent level of intrinsic DNA damage in cells derived from the MRL mouse. Similar to mouse ES cells, the p53-target p21 was not expressed in MRL ear fibroblasts. Because the p53/p21 axis plays a central role in the DNA damage response and cell cycle control, we directly tested the hypothesis that p21 down-regulation could functionally induce a regenerative response in an appendage of an otherwise nonregenerating mouse strain. Using the ear hole closure phenotype, a genetically mapped and reliable quantitative indicator of regeneration in the MRL mouse, we show that the unrelated Cdkn1atmi/Tyj/J p21?/? mouse (unlike the B6129SF2/J WT control) closes ear holes similar to MRL mice, providing a firm link between cell cycle checkpoint control and tissue regeneration. |
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