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

Am J Pathol. 2001 Nov;159(5):1681-8. doi: 10.1016/S0002-9440(10)63015-5.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

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


  • Plasminogen Activator Inhibitor 1