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MAP 4 regulates Tctex‐1 and promotes the migration of epidermal cells in hypoxia
Author(s) -
Chen Xin,
Zhou Xin,
Shi Xiaohua,
Xia Xin,
Zhang Yiming,
Fan Dongli
Publication year - 2018
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13763
Subject(s) - hacat , microbiology and biotechnology , cell migration , wound healing , blot , microtubule , transfection , cell , hypoxia (environmental) , chemistry , biology , cell culture , immunology , biochemistry , gene , oxygen , genetics , organic chemistry
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 DYNLT 1 (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 MAP 4 regulates microtubule dynamics and promotes epidermal cell migration through Tctex‐1. MAP 4 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.