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This phenotype is comparable to the human hemolytic anemia known as paroxysmal nocturnal hemoglobinuria (PNH), in which platelet activation and thrombosis play a critical pathogenic role. It has long been suspected but not formally demonstrated that both complement and nitric oxide (NO) contribute to PNH thrombosis. Using<jats:italic>mCd59a<\/jats:italic>and<jats:italic>mCd59b<\/jats:italic>double knockout mice (<jats:italic>mCd59ab<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice) in complement sufficient (<jats:italic>C3<\/jats:italic><jats:sup>+\/+<\/jats:sup>) and deficient (<jats:italic>C3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>) backgrounds, we document that<jats:italic>mCd59ab<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>platelets are sensitive to complement\u2010mediated activation and provide evidence for possible in vivo platelet activation in<jats:italic>mCd59ab<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice. Using a combination of L\u2010NAME (a NO\u2010synthase inhibitor) and NOC\u201018 or SNAP (NO\u2010donors), we further demonstrate that NO regulates complement\u2010mediated activation of platelets. These results indicate that the thrombotic diathesis of PNH patients could be due to a combination of increased complement\u2010mediated platelet activation and reduced NO\u2010bioavailability as a consequence of hemolysis. Am. J. Hematol. 2009. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ajh.21363","type":"journal-article","created":{"date-parts":[[2009,1,13]],"date-time":"2009-01-13T00:26:33Z","timestamp":1231806393000},"page":"221-227","source":"Crossref","is-referenced-by-count":26,"title":["Balancing role of nitric oxide in complement\u2010mediated activation of platelets from<i>mCd59a<\/i>and<i>mCd59b<\/i>double\u2010knockout 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