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凋亡诱导的代偿性增殖。细胞已死。细胞万岁!

Apoptosis-induced compensatory proliferation. The Cell is dead. Long live the Cell!

作者信息

Fan Yun, Bergmann Andreas

机构信息

Department of Biochemistry and Molecular Biology, University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.

出版信息

Trends Cell Biol. 2008 Oct;18(10):467-73. doi: 10.1016/j.tcb.2008.08.001. Epub 2008 Sep 4.

Abstract

In multi-cellular organisms, activation of apoptosis can trigger compensatory proliferation in surrounding cells to maintain tissue homeostasis. Genetic studies in Drosophila have indicated that distinct mechanisms of compensatory proliferation are employed in apoptotic tissues of different developmental states. In proliferating eye and wing tissues, the initiator caspase Dronc coordinates cell death and compensatory proliferation through the Jun N-terminal kinase and p53. The mitogens Decapentaplegic and Wingless are induced in this process. By contrast, in differentiating eye tissues, the effector caspases DrICE and Dcp-1 activate the Hedgehog signaling pathway to induce compensatory proliferation. In this review, we summarize these findings and discuss how activation of apoptosis is linked to the process of compensatory proliferation. The developmental and pathological relevance of compensatory proliferation is also discussed.

摘要

在多细胞生物中,细胞凋亡的激活可触发周围细胞的代偿性增殖,以维持组织内稳态。果蝇的遗传学研究表明,不同发育状态的凋亡组织采用了不同的代偿性增殖机制。在增殖的眼睛和翅膀组织中,起始半胱天冬酶Dronc通过Jun N端激酶和p53协调细胞死亡和代偿性增殖。在此过程中,有丝分裂原Decapentaplegic和Wingless被诱导产生。相比之下,在分化的眼睛组织中,效应半胱天冬酶DrICE和Dcp-1激活Hedgehog信号通路以诱导代偿性增殖。在这篇综述中,我们总结了这些发现,并讨论了细胞凋亡的激活如何与代偿性增殖过程相联系。我们还讨论了代偿性增殖在发育和病理方面的相关性。

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