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Related Collections Hemostasis, Thrombosis, and Vascular Biology Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 August 2002, Vol. 100, No. 3, pp. 917-924 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY NAD(P)H oxidase-dependent platelet superoxide anion release increases platelet recruitment Florian Krötz, Hae Young Sohn, Torsten Gloe, Stefan Zahler, Tobias Riexinger, Thomas M. Schiele, Bernhard F. Becker, Karl Theisen, Volker Klauss, and Ulrich Pohl From the Institute of Physiology and the Department of Internal Medicine, Ludwig-Maximilians-University Munich, Schillerstr 44, 80336 Munich, Germany, and Ziemssenstr 1, 80336 Munich, Germany. Platelets, although not phagocytotic, have been suggested to release O. Since O-producing reduced nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) oxidases can be specifically activated by certain agonists and are found in several nonphagocytotic tissues, we investigated whether such an enzyme is the source of platelet-derived O. We further studied which agonists cause platelet O release and whether platelet-derived O influences thrombus formation in vitro. Collagen, but not adenosine 5'-diphosphate (ADP) or thrombin, increased O formation in washed human platelets. This was a reduced nicotinamide adenine dinucleotide (NADH)-dependent process, as shown in platelet lysates. Consistent with a role of a platelet, NAD(P)H oxidase expression of its subunits p47phox and p67phox and inhibition of platelet O formation by diphenylene-iodoniumchloride (DPI) and by the specific peptide-antagonist gp91ds-tat were observed. Whereas platelet-derived O did not influence initial aggregation, platelet recruitment to a preformed thrombus following collagen stimulation was significantly attenuated by superoxide dismutase (SOD) or DPI. It was also inhibited when ADP released during aggregation was cleaved by the ectonucleotidase apyrase. ADP in supernatants of collagen-activated platelets was decreased in the presence of SOD, resulting in lower ADP concentrations available for recruitment of further platelets. Exogenous O increased ADP- concentrations in supernatants of collagen-stimulated platelets and induced irreversible aggregation when platelets were stimulated with otherwise subthreshold concentrations of ADP. These results strongly suggest that collagen activation induces NAD(P)H oxidase-dependent O release in platelets, which in turn enhances availability of released ADP, resulting in increased platelet recruitment. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F. Krotz, N. Hellwig, M. A. Burkle, S. Lehrer, T. Riexinger, H. Mannell, H.-Y. Sohn, V. Klauss, and U. Pohl A sulfaphenazole-sensitive EDHF opposes platelet-endothelium interactions in vitro and in the hamster microcirculation in vivo Cardiovasc Res, February 1, 2010; 85(3): 542 - 550. [Abstract] [Full Text] [PDF] D. Siegel-Axel, K. Daub, P. Seizer, S. Lindemann, and M. Gawaz Platelet lipoprotein interplay: trigger of foam cell formation and driver of atherosclerosis Cardiovasc Res, April 1, 2008; 78(1): 8 - 17. [Abstract] [Full Text] [PDF] J. E. 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