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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted 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 Taylor, F. J. Articles by Giles, A. R. Search for Related Content PubMed PubMed Citation Articles by Taylor, F. J. Articles by Giles, A. R. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Anticoagulant and fibrinolytic activities are promoted, not retarded, in vivo after thrombin generation in the presence of a monoclonal antibody that inhibits activation of protein C FB Taylor , H Hoogendoorn, AC Chang, G Peer, ME Nesheim, R Catlett, DC Stump and AR Giles Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City 73104. This study examines the assumption that both the anticoagulant and fibrinolytic activity that follow the generation of thrombin induced by infusion of factor Xa/PCPS are due to generation of activated protein C. Untreated controls or animals given unrelated antibody were compared with animals pretreated with a specific monoclonal antibody to protein C (HPC4). Compared with untreated controls excess HPC4 substantially reduced the level of protein C activation as observed by protein C immunoblotting and enzyme-linked immunosorbent assay for antitrypsin/activated protein C complexes. Despite this, the anticoagulant activity as reflected by the decline of factors Va and VIIIa levels (as observed by coagulation assays and by factor V immunoblotting) was significantly greater than controls. The fibrinolytic activity (as observed by assays of tissue plasminogen activator, D-Dimer, alpha 2-antiplasmin) also was significantly greater than controls. We conclude that neutralization of the protein C anticoagulant system while resulting in a significantly more intense coagulant response to Xa/PCPS does not preclude inactivation of factors Va and VIIIa and the full expression of the fibrinolytic response. We conclude further that after thrombin generation in vivo, protein C activation is not a prerequisite for the promotion of the fibrinolytic response previously observed, and that the inactivation of factors Va/VIIIa may be mediated by enzymes other than activated protein C. The reduction in alpha 2-antiplasmin levels in association with increased tissue plasminogen activator activity suggests that plasmin is a likely candidate. Volume 79, Issue 7, pp. 1720-1728, 04/01/1992 Copyright © 1992 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: K. Nogami, M. Shima, T. Matsumoto, K. Nishiya, I. Tanaka, and A. Yoshioka Mechanisms of Plasmin-catalyzed Inactivation of Factor VIII: A CRUCIAL ROLE FOR PROTEOLYTIC CLEAVAGE AT Arg336 RESPONSIBLE FOR PLASMIN-CATALYZED FACTOR VIII INACTIVATION J. Biol. Chem., February 23, 2007; 282(8): 5287 - 5295. [Abstract] [Full Text] [PDF] J. A. Samis, G. D. Ramsey, J. B. Walker, M. E. Nesheim, and A. R. Giles Proteolytic processing of human coagulation factor IX by plasmin Blood, February 1, 2000; 95(3): 943 - 951. [Abstract] [Full Text] [PDF] J. A. Samis, M. Garrett, R. P. Manuel, M. E. Nesheim, and A. R. Giles Human Neutrophil Elastase Activates Human Factor V but Inactivates Thrombin-Activated Human Factor V Blood, August 1, 1997; 90(3): 1065 - 1074. [Abstract] [Full Text] [PDF]

	Copyright © 1992 by American Society of Hematology         Online ISSN: 1528-0020