GADD34 suppresses wound healing by upregulating expression of myosin IIA
GADD34 suppresses wound healing by upregulating expression of myosin IIA
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DOI：
10.1007/s11248-009-9347-z
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发表时间：
2010-08
影响因子：
3
通讯作者：
C. Tanaka;S. Ito;N. Nishio;Y. Kodera;H. Sakurai;Haruhiko Suzuki;A. Nakao;K. Isobe
中科院分区：
文献类型：
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作者：
C. Tanaka;S. Ito;N. Nishio;Y. Kodera;H. Sakurai;Haruhiko Suzuki;A. Nakao;K. Isobe
伤口愈合包括组织修复的连续步骤，而细胞迁移尤为重要。为了分析生长停滞和DNA损伤诱导蛋白34(Gadd34)在组织修复中的潜在作用，我们进行了体外和体内创伤修复实验。在体外划痕实验中，Gadd34基因敲除(KO)的小鼠胚胎成纤维细胞(MEF)的迁移率高于野生型(WT)MEF。此外，Gadd34 KO MEF的伤口闭合速度快于WT MEF。通过活体穿孔活组织检查，与WT小鼠相比，Gadd34 KO小鼠的伤口愈合速度更快。与Gadd34KO小鼠相比，WT小鼠在迁移的巨噬细胞和肌成纤维细胞中表达更多的肌球蛋白IIA。这些结果表明，Gadd34通过肌球蛋白IIA的表达负性调节伤口愈合过程中的细胞迁移。
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.