神奇的P21關(guān)閉這種基因,，人體將可自愈并修復(fù)斷肢、背傷甚至腦損傷進(jìn)化的損失兩棲動(dòng)物能再生,，但其他動(dòng)物卻在進(jìn)化過程中失去了該能力斷肢,、背傷甚至腦損傷的自行修復(fù)在未來將成為現(xiàn)實(shí),。因?yàn)榭茖W(xué)家日前發(fā)現(xiàn)了一種基因,，該基因?qū)@種近乎神奇的能力起關(guān)鍵作用。
科學(xué)家發(fā)現(xiàn)p21基因阻礙了人體的自愈能力，而這種能力在包括兩棲動(dòng)物在內(nèi)的一些生物身上得以延續(xù),，但其他動(dòng)物卻在進(jìn)化過程中失去了該能力,。
關(guān)閉p21開啟再生
來自費(fèi)城維斯拓研究所的科研人員發(fā)現(xiàn)缺乏p21的老鼠獲得了再生其受損或缺失組織的能力,。與其他通過傷疤進(jìn)行愈合的典型哺乳動(dòng)物不同,，這些老鼠通過形成一種胚基來幫助細(xì)胞快速生長(zhǎng),。
研究人員發(fā)現(xiàn),，p21的缺失導(dǎo)致這些老鼠的細(xì)胞活動(dòng)更類似于胚胎干細(xì)胞而非成年哺乳動(dòng)物細(xì)胞,。這意味著它們將再生而非修復(fù)其軀體,。該發(fā)現(xiàn)發(fā)表于《國家科學(xué)院學(xué)報(bào)》PNAS上,為組織再生與細(xì)胞分裂控制的關(guān)聯(lián)提供了確鑿的證據(jù)。
科學(xué)家們?cè)诙渴軗p的老鼠身上關(guān)閉了p21基因,，之后這些老鼠的耳朵再生了,。
任何治療都可起效
首席科學(xué)家艾倫·赫博·卡茨教授指出，“就像斷肢的蠑螈一樣,，這些老鼠將會(huì)用健康的組織來取代那些受損甚至缺失的組織,，而且不會(huì)留下任何傷疤。”
“總有一天我們可以通過暫時(shí)失活p21以提高人體的再生能力。我們認(rèn)為任何未來療法都需要在治療過程中暫時(shí)關(guān)閉受傷位置上的p21,。這可能需要局部起效藥物才能達(dá)成,。而這將會(huì)把副作用降到最低。”（生物谷Bioon.com）
2010年干細(xì)胞技術(shù)與應(yīng)用講座
將邀請(qǐng)國內(nèi)外干細(xì)胞領(lǐng)域的頂級(jí)科研和臨床研究專家,，就干細(xì)胞培養(yǎng)/分化/重排/調(diào)控/臨床應(yīng)用方面進(jìn)行更多細(xì)化和更加深入的討論,。
生物谷推薦原文出處：
PNAS doi: 10.1073/pnas.1000830107
Lack of p21 expression links cell cycle control and appendage regeneration in mice
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
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.
