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

Abstract

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 wild-type (WT) and PAI-1(-/-) mice, the rate of wound closure is significantly accelerated in PAI-1(-/-) mice.

• Authors: J C Chan, D A Duszczyszyn, F J Castellino, V A Ploplis
• Journal: The American journal of pathology (Am J Pathol) Vol. 159 Issue 5 Pg. 1681-8 (Nov 2001) ISSN: 0002-9440 [Print] United States
• PMID: 11696429 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Plasminogen Activator Inhibitor 1

Topics

• Animals
• Kinetics
• Mice
• Mice, Inbred C57BL
• Mice, Knockout (genetics)
• Plasminogen Activator Inhibitor 1 (deficiency, genetics)
• Reference Values
• Skin (injuries, pathology, physiopathology)
• Time Factors
• Wound Healing (physiology)
• Wounds, Penetrating (pathology, physiopathology)