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After acute wound formation, the oxygen supply is reduced, which results in the formation of an acute hypoxic microenvironment; whether this hypoxic microenvironment enhances epidermal cell migration and the underlying regulatory molecular mechanism of this effect are unclear. In this study, HaCaT cells were maintained under hypoxic (1% oxygen) or normoxic conditions. Methods including immunofluorescence staining, wound scratch assays, transwell assays, Western blotting and high‐ and low‐expression lentiviral vector transfection were utilized to observe the changes in cell migration, microtubule dynamics and the expression levels of microtubule‐associated protein (MAP) 4 and the light chain protein DYNLT1 (Tctex‐1). The possible mechanisms were studied and discussed. The results showed that epidermal cell migration was enhanced during early hypoxia. Further experiments revealed that MAP4 regulates microtubule dynamics and promotes epidermal cell migration through Tctex‐1. MAP4 and Tctex‐1 play important roles in regulating the migration of epidermal cells under hypoxia. This evidence will provide a basis for further revealing the cellular and molecular mechanisms of local wound hypoxia and for promoting wound healing. [ABSTRACT FROM AUTHOR]

Objective To investigate the changes in the migration and motility of epidermal cells cultured under hypoxic conditions and the role of Gαi1 in promoting these changes. Methods A workstation for live cell imaging was used to observe the changes in the migration and motility of HaCaT cells cultured under hypoxic conditions for 24 h in comparison with cells in routine culture. Microarray chip technique was used to screen the differentially expressed genes that participated in the regulation of cell migration early after hypoxia exposure; Western blotting, immunofluorescence assay and lentivirus-mediated siRNA transfection were used to explore the role of Gαi1 protein in regulating the migration of HaCaT cells under hypoxic conditions. Results The migration ability of HaCaT cells was significantly enhanced under hypoxic conditions, and their movement rate and movement persistence were increased obviously early after hypoxic exposure (in the first 12 h) compared with the cells in normoxic culture. Western blotting and immunofluorescence assay showed that the exposure to hypoxia caused over-expression of Gαi1 protein in HaCaT cells. RNA interference of Gαi1 protein significantly lowered the migration ability of the cells irrespective of normoxic and hypoxic exposures and also resulted in obviously lowered cell motility and movement persistence. Conclusion Short-term hypoxic exposure significantly enhances the migration and movement of epidermal cells, and Gαi1 protein plays an important role in promoting the migration of epidermal cells under hypoxia.