Gutiérrez-Fernández Ana, Inada Masaki, Balbín Milagros, Fueyo Antonio, Pitiot Ana S, Astudillo Aurora, Hirose Kenji, Hirata Michiko, Shapiro Steven D, Noël Agnès, Werb Zena, Krane Stephen M, López-Otín Carlos, Puente Xose S
Departamento de Bioquímica y Biología Molecular, Universidad de Oviedo, 33006 Oviedo, Spain.
FASEB J. 2007 Aug;21(10):2580-91. doi: 10.1096/fj.06-7860com. Epub 2007 Mar 28.
Matrix metalloproteinases (MMPs) have been implicated in numerous tissue-remodeling processes. The finding that mice deficient in collagenase-2 (MMP-8) are more susceptible to develop skin cancer, prompted us to investigate the role of this protease in cutaneous wound healing. We have observed a significant delay in wound closure in MMP8-/- mice and an altered inflammatory response in their wounds, with a delay of neutrophil infiltration during the first days and a persistent inflammation at later time points. These changes were accompanied by alterations in the TGF-beta1 signaling pathway and by an apoptosis defect in MMP8-/- mice. The delay in wound healing observed in MMP8-/- mice was rescued by bone marrow transplantation from wild-type mice. Analysis of other MMPs showed that MMP8-/- mice had a significant increase in the expression of MMP-9, suggesting that both proteases might act coordinately in this process. This possibility was further supported by the novel finding that MMP-8 and MMP-9 form specific complexes in vivo. Taken together, these data indicate that MMP-8 participates in wound repair by contributing to the resolution of inflammation and open the possibility to develop new strategies for treating wound healing defects.
基质金属蛋白酶(MMPs)与众多组织重塑过程有关。缺乏胶原酶-2(MMP-8)的小鼠更易患皮肤癌,这一发现促使我们研究这种蛋白酶在皮肤伤口愈合中的作用。我们观察到MMP8 - / - 小鼠的伤口闭合明显延迟,其伤口的炎症反应改变,在最初几天中性粒细胞浸润延迟,在后期时间点炎症持续存在。这些变化伴随着TGF-β1信号通路的改变以及MMP8 - / - 小鼠的凋亡缺陷。从野生型小鼠进行骨髓移植可挽救MMP8 - / - 小鼠中观察到的伤口愈合延迟。对其他MMPs的分析表明,MMP8 - / - 小鼠中MMP-9的表达显著增加,这表明这两种蛋白酶可能在此过程中协同作用。MMP-8和MMP-9在体内形成特定复合物这一新发现进一步支持了这种可能性。综上所述,这些数据表明MMP-8通过促进炎症消退参与伤口修复,并为开发治疗伤口愈合缺陷的新策略提供了可能性。