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This Article Full Text Full Text (PDF) Supplemental Videos Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Kaul, D. K. Articles by Coller, B. S. Search for Related Content PubMed PubMed Citation Articles by Kaul, D. K. Articles by Coller, B. S. Related Collections Focus on Hematology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, Vol. 95 No. 2 (January 15), 2000: pp. 368-374 Monoclonal antibodies to V3 (7E3 and LM609) inhibit sickle red blood cell-endothelium interactions induced by platelet-activating factor D. K. Kaul, H. M. Tsai, X. D. Liu, M. T. Nakada, R. L. Nagel, and B. S. Coller From Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY; Centocor Inc, Malvern, PA; and Mount Sinai School of Medicine, New York, NY. Abnormal interaction of sickle red blood cells (SS RBC) with the vascular endothelium has been implicated as a factor in the initiation of vasoocclusion in sickle cell anemia. Both von Willebrand factor (vWf) and thrombospondin (TSP) play important roles in mediating SS RBC-endothelium interaction and can bind to the endothelium via V3 receptors. We have used monoclonal antibodies (MoAb) directed against V3 and IIb3 (GPIIb/IIIa) integrins to dissect the role of these integrins in SS RBC adhesion. The murine MoAb 7E3 inhibits both V3 and IIb3 (GPIIb/IIIa), whereas MoAb LM609 selectively inhibits V3, and MoAb 10E5 binds only to IIb3. In this study, we have tested the capacity of these MoAbs to block platelet-activating factor (PAF)-induced SS RBC adhesion in the ex vivo mesocecum vasculature of the rat. Infusion of washed SS RBC in preparations treated with PAF (200 pg/mL), with or without a control antibody, resulted in extensive adhesion of these cells in venules, accompanied by frequent postcapillary blockage and increased peripheral resistance units (PRU). PAF also caused increased endothelial surface and interendothelial expression of endothelial vWf. Importantly, pretreatment ofthe vasculature with either MoAb 7E3 F(ab')2 or LM609, but not 10E5 F(ab')2, after PAF almost completely inhibited SS RBC adhesion in postcapillary venules, the sites of maximal adhesion and frequent blockage. The inhibition of adhesion with 7E3 or LM609 was accompanied by smaller increases in PRU and shorter pressure-flow recovery times. Thus, blockade of V3 may constitute a potential therapeutic approach to prevent SS RBC-endothelium interactions under flow conditions. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. 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