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American Journal of Pathology, Vol 145, 33-36, Copyright © 1994 by American Society for Investigative Pathology

REGULAR ARTICLES

Anti-CD31 delays platelet adhesion/aggregation at sites of endothelial injury in mouse cerebral arterioles

WI Rosenblum, S Murata, GH Nelson, PK Werner, R Ranken and RC Harmon
Department of Pathology (Neuropathology), Virginia Commonwealth University, Medical College of Virginia, Richmond 23298-0017.

The arterioles on the surface of the mouse brain (pial arterioles) were observed by in vivo microscopy. A focus of minor endothelial damage was produced in a single pial arteriole in each mouse by briefly exposing the site to a helium neon laser after an intravenous injection of Evans blue. Mice were injected 10 minutes before injury with a monoclonal antibody (MAb) to mouse CD31, also known as platelet endothelial cell adhesion molecule. This treatment doubled (P < .01) the time required for the laser to produce a recognizable platelet aggregate. In additional experiments, an MAb to mouse CD61 and an MAb to mouse intercellular adhesion molecule 1 had no effect. The data support previous observations indicating that platelet adhesion/aggregation in this model is induced by endothelial injury without exposure of basal lamina. The data are consistent with the hypothesis that the endothelial injury exposes or activates a platelet endothelial cell adhesion molecule on the endothelium which is blocked by the MAb directed against CD31. This may be the first demonstration of an effect of an anti-platelet endothelial cell adhesion molecule on platelet endothelial cell adhesion molecule on platelet adhesion/aggregation in vivo.

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