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GADD34 suppresses wound healing by upregulating expression of myosin IIA
Authors:Chie Tanaka  Sachiko Ito  Naomi Nishio  Yasuhiro Kodera  Hidetoshi Sakurai  Haruhiko Suzuki  Akimasa Nakao  Ken-Ichi Isobe
Affiliation:(1) Department of Immunology, Nagoya University Graduate School of Medicine, 65 Turumai-cho, Showa-ku, Nagoya Aichi, 466-8520, Japan;(2) Department of Surgery II, Nagoya University Graduate School of Medicine, 65 Turumai-cho, Showa-ku, Nagoya Aichi, 466-8520, Japan;
Abstract:Wound healing consists of sequential steps of tissue repair, and cell migration is particularly important. In order to analyze the potential function of growth arrest and DNA damage inducible protein 34 (GADD34) in tissue repair, we performed in vitro and in vivo wound healing experiments. In an in vitro scratch assay, GADD34 knockout (KO) mouse embryonic fibroblasts (MEFs) had higher migration rates than did wild type (WT) MEFs. Furthermore, the rate of wound closure was faster in GADD34 KO MEFs than in WT MEFs. Using in vivo punch biopsy assays, GADD34 KO mice had accelerated wound healing compared to WT mice. WT mice expressed higher amounts of myosin IIA in migrating macrophages and myofibroblasts than did GADD34 KO mice. These results indicate that GADD34 negatively regulates cell migration in wound healing via expression of myosin IIA.
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