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首页> 美国卫生研究院文献>Journal of the Boston Society of Medical Sciences >MMP-13 Plays a Role in Keratinocyte Migration Angiogenesis and Contraction in Mouse Skin Wound Healing
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MMP-13 Plays a Role in Keratinocyte Migration Angiogenesis and Contraction in Mouse Skin Wound Healing

机译：MMP-13在小鼠皮肤伤口愈合中在角质形成细胞迁移血管生成和收缩中发挥作用。

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Matrix metalloproteinases (MMPs) have been implicated in wound healing. To analyze the roles of MMP-9 and MMP-13 in wound healing, we generated full-thickness cutaneous wounds in MMP-9 knockout (KO), MMP-13 KO, MMP-9/13 double KO, and wild-type mice. Macroscopic wound closure was delayed in all of the KO mice, as compared with wild-type mice. The rate of re-epithelialization was significantly delayed in MMP-9 KO and MMP-13 KO mice and remarkably delayed in MMP-9/13 double KO mice, as compared with wild-type mice. Both MMP-9 and MMP-13 were expressed by the leading edges of epidermal cells in wild-type mice, and the migration of keratinocytes was suppressed by treatment with an MMP inhibitor or transfection of small interfering RNAs for MMP-9 or MMP-13, as compared with controls. The vascular density in wound granulation was significantly lower in both MMP-13 KO and MMP-9/13 double KO mice than in wild-type mice. Degradation of connective tissue growth factor in wound tissue was transiently prevented in MMP-13 KO mice. Morphometric analyses demonstrated a reduction in both wound contraction and myofibroblast formation in both MMP-13 KO and MMP-9/13 double KO mice. Proliferation and transforming growth factor-β1-induced myofibroblast differentiation of dermal fibroblasts from MMP-13 KO mice were decreased, as compared with wild-type dermal fibroblasts. These data suggest that MMP-13 plays a role in keratinocyte migration, angiogenesis, and contraction in wound healing, while MMP-9 functions in keratinocyte migration.
机译：基质金属蛋白酶（MMPs）已牵涉伤口愈合。为了分析MMP-9和MMP-13在伤口愈合中的作用，我们在MMP-9敲除（KO），MMP-13 KO，MMP-9 / 13 double KO和野生型小鼠中产生了全层皮肤伤口。与野生型小鼠相比，所有KO小鼠的宏观伤口闭合延迟。与野生型小鼠相比，MMP-9 KO和MMP-13 KO小鼠的重新上皮形成速率显着延迟，而MMP-9 / 13 double KO小鼠的显着延迟。 MMP-9和MMP-13均在野生型小鼠的表皮细胞前沿表达，并且通过使用MMP抑制剂处理或转染MMP-9或MMP-13的小干扰RNA抑制了角质形成细胞的迁移。 ，与控件相比。 MMP-13 KO和MMP-9 / 13 double KO小鼠的伤口肉芽形成中的血管密度均显着低于野生型小鼠。在MMP-13 KO小鼠中，瞬时预防了伤口组织中结缔组织生长因子的降解。形态分析表明，MMP-13 KO和MMP-9 / 13 double KO小鼠的伤口收缩和成肌纤维细胞形成均减少。与野生型真皮成纤维细胞相比，MMP-13 KO小鼠的真皮成纤维细胞的增殖和转化生长因子-β1诱导的肌成纤维细胞分化减少。这些数据表明，MMP-13在伤口愈合中在角质形成细胞迁移，血管生成和收缩中起作用，而MMP-9在角质形成细胞迁移中起作用。

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