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胶原酶的表皮表达会延缓转基因小鼠的伤口愈合。

Epidermal expression of collagenase delays wound-healing in transgenic mice.

作者信息

Di Colandrea T, Wang L, Wille J, D'Armiento J, Chada K K

机构信息

Department of Biochemistry, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway 08854, USA.

出版信息

J Invest Dermatol. 1998 Dec;111(6):1029-33. doi: 10.1046/j.1523-1747.1998.00457.x.

DOI:10.1046/j.1523-1747.1998.00457.x
PMID:9856812
Abstract

A vital characteristic of skin is its ability for wound repair in response to injury. A transient elevation of matrix metalloproteinases (MMP) in the epidermal and dermal compartments of healing wounds implicates the MMP family of enzymes in the regulation of events important to injury repair. Transgenic mice expressing human interstitial collagenase (MMP-1) in the epidermis were used to perturb the regulation of this proteinase in order to examine the role of epidermal collagenase during wound healing. The relative healing potential of collagenase transgenic mice and wild-type littermates was assessed by measurements of the wound area during closure of full-thickness wounds. Transgenic mice exhibited a 2-3 d delay in the time required to reach 50% closure of 6 mm wounds. Histologic analysis of the transgenic wound bed revealed the retarded migration of the epithelium across the open wound. The results are consistent with the hypothesis that control of collagenase (MMP-1) expression is important for re-epithelialization during wound healing and indicate that collagenase regulation is critical to the kinetics of normal wound closure.

摘要

皮肤的一个重要特性是其在受伤后进行伤口修复的能力。愈合伤口的表皮和真皮层中基质金属蛋白酶(MMP)的短暂升高表明,MMP酶家族参与了对损伤修复重要事件的调节。利用在表皮中表达人间质胶原酶(MMP-1)的转基因小鼠来扰乱这种蛋白酶的调节,以便研究表皮胶原酶在伤口愈合过程中的作用。通过测量全层伤口闭合期间的伤口面积,评估了胶原酶转基因小鼠和野生型同窝小鼠的相对愈合潜力。转基因小鼠在6毫米伤口达到50%闭合所需的时间上延迟了2至3天。对转基因伤口床的组织学分析显示,上皮细胞在开放性伤口上的迁移受阻。这些结果与以下假设一致,即胶原酶(MMP-1)表达的控制对伤口愈合过程中的再上皮化很重要,并表明胶原酶调节对正常伤口闭合的动力学至关重要。

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