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© 2019. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

Both cell migration and proliferation are indispensable parts of reepithelialization during skin wound healing, which is a complex process for which the underlying molecular mechanisms are largely unknown. Here, we identify a novel role for microtubule-associated protein 4 (MAP4), a cytosolic microtubule-binding protein that regulates microtubule dynamics through phosphorylation modification, as a critical regulator of epidermal wound repair. We showed that MAP4 phosphorylation was induced in skin wounds. In an aberrant phosphorylated MAP4 mouse model, hyperphosphorylation of MAP4 (S737 and S760) accelerated keratinocyte migration and proliferation and skin wound healing. Data from both primary cultured keratinocytes and HaCaT cells in vitro revealed the same results. The promigration and proproliferation effects of MAP4 phosphorylation depended on microtubule rearrangement and could be abolished by MAP4 dephosphorylation. We also identified p38/MAPK as an upstream regulator of MAP4 phosphorylation in keratinocytes. Our findings provide new insights into the molecular mechanisms underlying wound-associated keratinocyte migration and proliferation and identify potential targets for the remediation of defective wound healing.

Details

Title
Microtubule-associated protein 4 phosphorylation regulates epidermal keratinocyte migration and proliferation
Author
Zhang, Junhui; Li, Lingfei; Zhang, Qiong; Wang, Wensheng; Zhang, Dongxia; Jia, Jiezhi; Lv, Yanling; Yuan, Hongping; Song, Huapei; Xiang, Fei; Hu, Jiongyu; Huang, Yuesheng
Pages
1962-1976
Section
Research Papers
Publication year
2019
Publication date
2019
Publisher
Ivyspring International Publisher Pty Ltd
e-ISSN
1449-2288
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2598426470
Copyright
© 2019. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.