BNIP3 promotes the motility and migration of keratinocyte under hypoxia

The migration of keratinocytes from wound margins plays a critical role in the re‐epithelialization of skin wounds. Hypoxia occurs immediately after injury and acts as an early stimulus to initiate the healing processes. Although our previous studies have revealed that hypoxia promotes keratinocyte...

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Bibliographic Details
Published in:Experimental dermatology 2017-05, Vol.26 (5), p.416-422
Main Authors: Zhang, Junhui, Zhang, Dongxia, Yan, Tiantian, Jiang, Xupin, Zhang, Can, Zhao, Liping, Li, Lingfei, Tang, Di, Zhang, Qiong, Jia, Jiezhi, Zhang, Jiaping, Huang, Yuesheng
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
BNIP3
BNIP3 protein
Cell adhesion & migration
Cell migration
cell motility
Cell Movement
Cells, Cultured
Focal adhesion kinase
Focal Adhesion Kinase 1 - metabolism
Hypoxia
Hypoxia - metabolism
Keratinocytes
Keratinocytes - physiology
Membrane Proteins - metabolism
Mice, Inbred BALB C
Mitochondrial Proteins - metabolism
Molecular modelling
Signal Transduction
Skin
Wound healing
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Summary:The migration of keratinocytes from wound margins plays a critical role in the re‐epithelialization of skin wounds. Hypoxia occurs immediately after injury and acts as an early stimulus to initiate the healing processes. Although our previous studies have revealed that hypoxia promotes keratinocyte migration, the precise mechanisms involved remain unclear. Here, we found that BNIP3 expression was upregulated in hypoxic keratinocytes, and BNIP3 silencing suppressed hypoxia‐induced cell migration. Additionally, hypoxia activated the focal adhesion kinase (FAK) pathway through upregulation of BNIP3, while FAK inhibition attenuated hypoxic keratinocyte migration. Here, we conclusively demonstrate a novel role for BNIP3 in hypoxia‐induced keratinocyte migration. Furthermore, we provide a new perspective on the molecular mechanisms of wound healing and identify BNIP3 as a potential new molecular target for clinical treatments to enhance wound healing.
ISSN:0906-6705
1600-0625
DOI:10.1111/exd.13248