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凋亡细胞激活“凤凰涅槃”通路,促进伤口愈合和组织再生。

Apoptotic cells activate the "phoenix rising" pathway to promote wound healing and tissue regeneration.

机构信息

Department of Radiation Oncology, University of Colorado School of Medicine, Aurora, CO 80045, USA.

出版信息

Sci Signal. 2010 Feb 23;3(110):ra13. doi: 10.1126/scisignal.2000634.

DOI:10.1126/scisignal.2000634
PMID:20179271
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2905599/
Abstract

The ability to regenerate damaged tissues is a common characteristic of multicellular organisms. We report a role for apoptotic cell death in promoting wound healing and tissue regeneration in mice. Apoptotic cells released growth signals that stimulated the proliferation of progenitor or stem cells. Key players in this process were caspases 3 and 7, proteases activated during the execution phase of apoptosis that contribute to cell death. Mice lacking either of these caspases were deficient in skin wound healing and in liver regeneration. Prostaglandin E(2), a promoter of stem or progenitor cell proliferation and tissue regeneration, acted downstream of the caspases. We propose to call the pathway by which executioner caspases in apoptotic cells promote wound healing and tissue regeneration in multicellular organisms the "phoenix rising" pathway.

摘要

再生受损组织的能力是多细胞生物的共同特征。我们报告了细胞凋亡在促进小鼠伤口愈合和组织再生中的作用。凋亡细胞释放生长信号,刺激祖细胞或干细胞的增殖。这个过程中的关键参与者是半胱天冬酶 3 和 7,凋亡执行阶段激活的蛋白酶,有助于细胞死亡。缺乏这些半胱天冬酶之一的小鼠在皮肤伤口愈合和肝脏再生方面存在缺陷。前列腺素 E2(促进干细胞或祖细胞增殖和组织再生的物质)是半胱天冬酶的下游物质。我们建议将执行半胱天冬酶在凋亡细胞中促进多细胞生物伤口愈合和组织再生的途径称为“凤凰涅槃”途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/d06cb157f027/nihms206721f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/cd6520e3b6ba/nihms206721f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/22c984046bd6/nihms206721f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/a7b5318a3e07/nihms206721f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/67487eb89dd1/nihms206721f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/d06cb157f027/nihms206721f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/cd6520e3b6ba/nihms206721f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/a32f027bbb7c/nihms206721f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/22c984046bd6/nihms206721f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/a7b5318a3e07/nihms206721f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/67487eb89dd1/nihms206721f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e163/2905599/d06cb157f027/nihms206721f6.jpg

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Genetic interaction of PGE2 and Wnt signaling regulates developmental specification of stem cells and regeneration.
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