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首页> 外文期刊>Molecular biology of the cell >Activities of the matrix metalloproteinase stromelysin-2 (MMP-10) in matrix degradation and keratinocyte organization in wounded skin
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Activities of the matrix metalloproteinase stromelysin-2 (MMP-10) in matrix degradation and keratinocyte organization in wounded skin

机译：基质金属蛋白酶stromelysin-2（MMP-10）在伤口皮肤基质降解和角质形成细胞组织中的活性

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摘要

The matrix metalloproteinase stromelysin-2 is expressed in keratinocytes of the epithelial tongue of skin wounds, suggesting a role in keratinocyte migration. Here, we show that stromelysin-2 enhances migration of cultured keratinocytes. To gain insight into the in vivo activities of stromelysin-2 in epithelial repair, we generated transgenic mice expressing a constitutively active stromelysin-2 mutant in keratinocytes. These animals had no alterations in skin architecture, and the healing rate of skin wounds was normal. Histologically, however, we found abnormalities in the organization of the wound epithelium. Keratinocytes at the migrating epidermal tip were scattered in most sections of mice with high expression level, and there was a reduced deposition of new matrix. In particular, the staining pattern of laminin-5 at the wound site was altered. This may be due to proteolytic processing of laminin-5 by stromelysin-2, because degradation of laminin-5 by this enzyme was observed in vitro. The inappropriate matrix contact of keratinocytes was accompanied by aberrant localization of beta1-integrins and phosphorylated focal adhesion kinase, as well as by increased apoptosis of wound keratinocytes. These results suggest that a tightly regulated expression level of stromelysin-2 is required for limited matrix degradation at the wound site, thereby controlling keratinocyte migration.
机译：基质金属蛋白酶stromelysin-2在皮肤伤口上皮舌的角质形成细胞中表达，提示其在角质形成细胞迁移中的作用。在这里，我们显示stromelysin-2增强了培养的角质形成细胞的迁移。为了深入了解Stromelysin-2在上皮修复中的体内活性，我们生成了在角质形成细胞中表达组成型活性Stromelysin-2突变体的转基因小鼠。这些动物的皮肤结构没有改变，皮肤伤口的愈合速度正常。但是，从组织学上看，我们发现伤口上皮的组织异常。在迁移的表皮尖端处的角质形成细胞散布在大多数小鼠中，且表达水平较高，并且新基质的沉积减少。特别地，层粘连蛋白5在伤口部位的染色模式被改变。这可能是由于Stromelysin-2对laminin-5的蛋白水解作用所致，因为在体外观察到该酶对laminin-5的降解。角质形成细胞的不适当的基质接触伴随着β1-整联蛋白和磷酸化的粘着斑激酶的异常定位，以及伤口角质形成细胞的凋亡增加。这些结果表明，在伤口部位有限的基质降解需要严格调控stromelysin-2的表达水平，从而控制角质形成细胞的迁移。

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