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Blood, 9 July 2009, Vol. 114, No. 2, pp. 478-484. Prepublished online as a Blood First Edition Paper on May 6, 2009; DOI 10.1182/blood-2008-11-188763.
Submitted November 10, 2008
MediCity Research Laboratory and Department of Medical Microbiology, University of Turku and National Public Health Institute, Turku, Finland * Corresponding author; email: sirpa.jalkanen{at}utu.fi.
"Pathologische anatomie leiden endothelium" (PAL-E) antibody has been used for over 20 years as a marker for vascular endothelium. Despite its widespread use the target of this antibody was only recently identified as "plasmalemma vesicle associated protein-1" (PV-1). However, thus far no function has been identified for this molecule. Here we report that activation of human umbilical vein endothelial cells (HUVECs) with TNF-
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| Copyright © 2009 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
resulted in a remarkable redistribution of PV-1 towards the peripheral areas of the cells. Furthermore, in vitro end point transmigration experiments showed that transcellularly migrating lymphocytes are surrounded by rings containing PV-1 and caveolin-1. Moreover, PV-1 physically associates with vimentin. In addition, administration of anti PV-1 antibody during capillary flow assays resulted in a significant inhibition of lymphocyte transmigration through the endothelial cell layer, while rolling and adhesion were unaffected. In vivo blockage of PV-1 by an antibody in acute peritonitis and air pouch model resulted in a significant decrease in the number of migrating leukocytes. Here we thus define leukocyte transendothelial migration as the first known function for PV-1.
