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1 Blood Research Institute, The Blood Center of Southeastern Wisconsin, Milwaukee, WI, USA
2 Blood Research Institute, The Blood Center of Southeastern Wisconsin, Milwaukee, WI, USA; Cellular Biology, Medical College of Wisconsin, Milwaukee, WI, USA
3 Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
4 Blood Research Institute, The Blood Center of Southeastern Wisconsin, Milwaukee, WI, USA; Microbiology, Medical College of Wisconsin, Milwaukee, WI, USA
5 Blood Research Institute, The Blood Center of Southeastern Wisconsin, Milwaukee, WI, USA; Pharmacology, Medical College of Wisconsin, Milwaukee, WI, USA; The Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: pjnewman{at}bcsew.edu.
Platelet Endothelial Cell Adhesion Molecule-1 (PECAM-1; CD31) is a 130 kDa member of the immunoglobulin superfamily that is expressed on platelets and leukocytes, and is highly enriched at endothelial cell-cell junctions. Previous studies have shown that this vascular cell adhesion and signaling receptor functions to regulate platelet activation and thrombosis, to suppress apoptotic cell death, to mediate transendothelial migration of leukocytes, and to maintain the integrity of the vasculature. Since systemic exposure to the bacterial endotoxin, lipopolysaccharide (LPS) triggers an acute inflammatory response that involves many of these same processes, we compared the patho-physiological responses of wild-type versus PECAM-1-deficient mice to LPS challenge. We found that PECAM-1-deficient mice were significantly more sensitive to systemic LPS administration than were their wild-type counterparts, and that the lack of PECAM-1 expression at endothelial cell-cell junctions could account for the majority of the increased LPS-induced mortality observed. The diverse functional roles played by PECAM-1 in thrombosis, inflammation, apoptosis, and the immune response may make this molecule an attractive target for the development of novel therapeutics to manage and treat endotoxic shock.
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