Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 159, Issue 5, Pages 1681-1688Publisher
AMER SOC INVESTIGATIVE PATHOLOGY, INC
DOI: 10.1016/S0002-9440(10)63015-5
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- NHLBI NIH HHS [R01 HL063682, R01 HL013423, HL-63682, R37 HL013423, HL-13423] Funding Source: Medline
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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.
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