© 1996 American Heart Association, Inc.
Articles |
Migration of Arterial Wall Cells
Expression of Plasminogen Activators and Inhibitors in Injured Rat Arteries
From the Department of Pathology (M.A.R., C.I.), University of Washington, Seattle, and the Maine Medical Center Research Institute (V.L.), South Portland, Me.
Correspondence to Michael A. Reidy, PhD, University of Washington/Department of Pathology, Vascular Biology/Box 357335, Seattle, WA 98195-7335.
Abstract The expression of plasminogen activators and inhibitors was examined in denuded arteries. Within 5 days, smooth muscle cells (SMCs) on the luminal surface expressed the mRNA for tissue-type plasminogen activator (TPA), urokinase-type plasminogen activator (UPA), the receptor for UPA (UPAR), and plasminogen activator inhibitor type-1 (PAI-1). Similar results were seen after 8 days. Six weeks later, only TPA mRNA was still expressed by SMCs on the luminal surface. En face casein zymograms revealed a net fibrinolytic activity in areas covered with luminal SMCs. Reverse zymography showed no antifibrinolytic activity in these zones. Quiescent endothelial cells did not express TPA, UPA, UPAR, or PAI-1 mRNA. Regenerating endothelium at the wound edge strongly expressed TPA, UPA, and UPAR, as well as PAI-1. UPA and UPAR expression was highly restricted to cells at the wound edge and was not present elsewhere. En face zymography showed no plasmin activity in endothelialized areas, and reverse zymography showed a net antifibrinolytic activity in endothelialized zones. These results suggest that plasminogen activator and inhibitor expression correlates with the migration of both SMCs and endothelial cells into an arterial wound.
Key Words: arterial injury • plasminogen activators • smooth muscle cells • endothelium
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