美国科学家发现，关闭了耳朵遭受重创的小鼠的p21基因后，小鼠能够重新长出耳朵。研究人员表示，该方法可能也适用于人类，或许某一天，人类也能够实现断肢再生。相关研究发表于最新一期的美国《国家科学院院刊》（PNAS）上。
美国费城威斯达研究所的研究人员表示，他们很早就知道，p21基因对40多种与DNA复制和细胞分裂有关的基因有干扰作用，它会阻碍生物体伤患处的治愈过程。因此，关闭p21基因可以恢复某些动物重新长出新的身体组织的能力。
在实验中，研究人员关闭了耳朵受损的小鼠的p21基因，结果发现小鼠重新长出了耳朵。但与典型的哺乳动物通过结疤治愈伤口不同，p21基因关闭后，小鼠耳朵伤口周围刚开始会产生一堆名为“芽基”的细胞，这些细胞并不发展成单一的结疤组织，而是聚集起来继续分化，每个细胞朝不同的组织类型发展，如骨骼、肌肉、神经等，最终形成新的身体组织。
该研究的负责人、威斯达学院的艾伦赫柏-凯兹认为，新研究明确地证明，身体组织的再生与控制细胞的分裂相关。尽管这项研究目前还处于初级阶段，但从理论上来说，这个过程也同样适用于人类。或许某一天，我们仅通过关闭p21基因就可加速人类身体组织的治愈过程，重新长出被截断了的四肢、受损的背部甚至遭受重创的大脑，而且副作用更少。
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《国家科学院院刊》发表论文摘要（英文）
Published online before print March 15, 2010, 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
Abstract
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.
