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缺氧通过P38/丝裂原活化蛋白激酶途径调节CD9介导的角质形成细胞迁移。

Hypoxia regulates CD9-mediated keratinocyte migration via the P38/MAPK pathway.

作者信息

Jiang Xupin, Guo Xiaowei, Xu Xue, Teng Miao, Huang Chong, Zhang Dongxia, Zhang Qiong, Zhang Jiaping, Huang Yuesheng

机构信息

Institute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, The Third Military Medical University, Chongqing, China.

The No. 324 Hospital of PLA, Chongqing, China.

出版信息

Sci Rep. 2014 Sep 9;4:6304. doi: 10.1038/srep06304.

DOI:10.1038/srep06304
PMID:25200404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4158574/
Abstract

Keratinocyte migration is an early event in the wound healing process. Although we previously found that CD9 downregulation is required for the keratinocyte migration during wound repair, the mechanism of how CD9 expression is regulated remains unclear. Here, we observed the effect of hypoxia (2% O2) on CD9 expression and keratinocyte migration. CD9 expression was downregulated and keratinocyte migration was increased under hypoxic conditions. In addition, CD9 overexpression reversed hypoxia-induced cell migration. We also found that hypoxia activated the p38/MAPK pathway. SB203580, a p38/MAPK inhibitor, increased CD9 expression and inhibited keratinocyte migration under hypoxia, while MKK6 (Glu) overexpression decreased CD9 expression and promoted hypoxic keratinocyte migration. Our results demonstrate that hypoxia regulates CD9 expression and CD9-mediated keratinocyte migration via the p38/MAPK pathway.

摘要

角质形成细胞迁移是伤口愈合过程中的早期事件。尽管我们之前发现伤口修复过程中角质形成细胞迁移需要CD9下调，但其表达调控机制仍不清楚。在此，我们观察了缺氧（2%氧气）对CD9表达和角质形成细胞迁移的影响。在缺氧条件下，CD9表达下调，角质形成细胞迁移增加。此外，CD9过表达逆转了缺氧诱导的细胞迁移。我们还发现缺氧激活了p38/丝裂原活化蛋白激酶（MAPK）通路。p38/MAPK抑制剂SB203580在缺氧条件下增加CD9表达并抑制角质形成细胞迁移，而MKK6（谷氨酸）过表达降低CD9表达并促进缺氧角质形成细胞迁移。我们的结果表明，缺氧通过p38/MAPK通路调节CD9表达和CD9介导的角质形成细胞迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54e9/4158574/ad8dcba8d53d/srep06304-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54e9/4158574/9827aefbb44d/srep06304-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54e9/4158574/b0cb1985bd8a/srep06304-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54e9/4158574/ac9db507b415/srep06304-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54e9/4158574/5187c5f8d22a/srep06304-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54e9/4158574/ad8dcba8d53d/srep06304-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54e9/4158574/9827aefbb44d/srep06304-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54e9/4158574/b0cb1985bd8a/srep06304-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54e9/4158574/ac9db507b415/srep06304-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54e9/4158574/5187c5f8d22a/srep06304-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54e9/4158574/ad8dcba8d53d/srep06304-f5.jpg

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