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

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作者
Xupin Jiang
Xiaowei Guo
Xue Xu
Miao Teng
Chong Huang
Dongxia Zhang
Qiong Zhang
Jiaping Zhang
Yuesheng Huang
机构
[1] Institute of Burn Research,Department of Burn and Plastic Surgery
[2] State Key Laboratory of Trauma,undefined
[3] Burns and Combined Injury,undefined
[4] Southwest Hospital,undefined
[5] The Third Military Medical University,undefined
[6] The No. 324 Hospital of PLA,undefined
[7] The First Affiliated Hospital of Chongqing Medical University,undefined
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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.
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