Accelerated skin wound healing in plasminogen activator inhibitor-1-deficient mice

被引：94
作者：
Chan, JCY
Duszczyszyn, DA
Castellino, FJ
Ploplis, VA
机构：
[1] Univ Notre Dame, WM Keck Ctr Transgene Res, Notre Dame, IN 46556 USA
[2] Univ Notre Dame, Dept Chem & Biochem, Notre Dame, IN 46556 USA
来源：
AMERICAN JOURNAL OF PATHOLOGY | 2001年 / 159卷 / 05期
关键词：
D O I：
10.1016/S0002-9440(10)63015-5
中图分类号：
R36 [病理学];
学科分类号：
100104 ;
摘要：
Components of the fibrinolytic system have been implicated in cell migratory events associated with tissue remodeling. Studies in plasminogen-deficient mice (PG(-/-)) indicated that skin wound healing is impaired, but is resolved with an additional fibrinogen deficiency. Plasminogen activator inhibitor-1 (PAI-1) expression by keratinocytes has been identified shortly after wound injury. PAI-1 expression could affect wound healing by regulating the fibrinolytic environment of the wounded area, as well as influencing events associated with cell attachment and detachment through interactions with matrix proteins. The present study directly assesses PAI-1 involvement In skin wound healing through analyses of a dermal biopsy punch model in PAI-1-deficient (PAI-1(-/-)) mice. While the cellular events associated with the healing process are similar between wildtype (WT) and PAI-1(-/-) mice, the rate of wound closure is significantly accelerated in PAI-1(-/-) mice.
引用
收藏
页码：1681 / 1688
页数：8
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