期刊
JOURNAL OF CELL SCIENCE
卷 126, 期 9, 页码 1942-1951出版社
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.113225
关键词
Keratinocyte; Directional migration; ENaC; Lamellipodia
类别
资金
- National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health (NIH) [R01AR044518]
- BBSRC [BB/E013597/1] Funding Source: UKRI
- MRC [MR/K012770/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/E013597/1] Funding Source: researchfish
- Medical Research Council [MR/K012770/1] Funding Source: researchfish
Cellular directional migration in an electric field (galvanotaxis) is one of the mechanisms guiding cell movement in embryogenesis and in skin epidermal repair. The epithelial sodium channel (ENaC), in addition to its function of regulating sodium transport in kidney, has recently been found to modulate cell locomotory speed. Here we tested whether ENaC has an additional function of mediating the directional migration of galvanotaxis in keratinocytes. Genetic depletion of ENaC completely blocks only galvanotaxis and does not decrease migration speed. Overexpression of ENaC is sufficient to drive galvanotaxis in otherwise unresponsive cells. Pharmacologic blockade or maintenance of the open state of ENaC also decreases or increases, respectively, galvanotaxis, suggesting that the channel open state is responsible for the response. Stable lamellipodial extensions formed at the cathodal sides of wild-type cells at the start of galvanotaxis; these were absent in the ENaC knockout keratinocytes, suggesting that ENaC mediates galvanotaxis by generating stable lamellipodia that steer cell migration. We provide evidence that ENaC is required for directional migration of keratinocytes in an electric field, supporting a role for ENaC in skin wound healing.
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