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创伤触发 MIRO-1 依赖性线粒体片段化，通过氧化信号加速表皮伤口闭合。

Wounding triggers MIRO-1 dependent mitochondrial fragmentation that accelerates epidermal wound closure through oxidative signaling.

机构信息

Center for Stem Cell and Regenerative Medicine and Department of Cardiology of The Second Affiliated Hospital, Zhejiang University School of Medicine, 310058, Hangzhou, China.

The Zhejiang University-University of Edinburgh Institute, 718 East Haizhou Rd., Haining, 314400, Zhejiang, China.

出版信息

Nat Commun. 2020 Feb 26;11(1):1050. doi: 10.1038/s41467-020-14885-x.

DOI:10.1038/s41467-020-14885-x
PMID:32103012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7044169/
Abstract

Organisms respond to tissue damage through the upregulation of protective responses which restore tissue structure and metabolic function. Mitochondria are key sources of intracellular oxidative metabolic signals that maintain cellular homeostasis. Here we report that tissue and cellular wounding triggers rapid and reversible mitochondrial fragmentation. Elevated mitochondrial fragmentation either in fzo-1 fusion-defective mutants or after acute drug treatment accelerates actin-based wound closure. Wounding triggered mitochondrial fragmentation is independent of the GTPase DRP-1 but acts via the mitochondrial Rho GTPase MIRO-1 and cytosolic Ca. The fragmented mitochondria and accelerated wound closure of fzo-1 mutants are dependent on MIRO-1 function. Genetic and transcriptomic analyzes show that enhanced mitochondrial fragmentation accelerates wound closure via the upregulation of mtROS and Cytochrome P450. Our results reveal how mitochondrial dynamics respond to cellular and tissue injury and promote tissue repair.

摘要

生物体通过上调保护性反应来应对组织损伤，这些反应恢复组织结构和代谢功能。线粒体是维持细胞内稳态的细胞内氧化代谢信号的关键来源。在这里，我们报告组织和细胞损伤会引发快速和可逆的线粒体片段化。在 fzo-1 融合缺陷突变体中或在急性药物处理后，线粒体片段化的升高会加速肌动蛋白为基础的伤口闭合。由损伤触发的线粒体片段化与 GTPase DRP-1 无关，但通过线粒体 Rho GTPase MIRO-1 和细胞质 Ca 起作用。fzo-1 突变体的碎片化线粒体和加速的伤口闭合依赖于 MIRO-1 的功能。遗传和转录组分析表明，增强的线粒体片段化通过上调 mtROS 和细胞色素 P450 加速伤口闭合。我们的结果揭示了线粒体动力学如何响应细胞和组织损伤并促进组织修复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/719d/7044169/9f724f9a21d3/41467_2020_14885_Fig7_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/719d/7044169/9f724f9a21d3/41467_2020_14885_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/719d/7044169/ef6d9f6e9fc6/41467_2020_14885_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/719d/7044169/135676f4ccd6/41467_2020_14885_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/719d/7044169/249f2df1ed70/41467_2020_14885_Fig3_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/719d/7044169/cb76b5edc5e0/41467_2020_14885_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/719d/7044169/60205f5c7645/41467_2020_14885_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/719d/7044169/9f724f9a21d3/41467_2020_14885_Fig7_HTML.jpg

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