한빛사 논문
Abstract
1Division of Hemostasis and Thrombosis, Beth Israel Deaconess
Medical Center and Harvard Medical School, Boston, Massachusetts, USA.
2Cardiovascular
Research Institute, University of California San Francisco, San Francisco, California,
USA.
Address correspondence to: Bruce Furie, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, Massachusetts 02215, USA. Phone: (617) 754-1200; Fax: (617) 754-1234.
Published February 21, 2008
Received for publication October 3, 2007,
and accepted in revised form January 30, 2008.
Abstract
Thiol isomerases, including protein disulfide isomerase (PDI), catalyze disulfide oxidation, reduction, and isomerization, thereby playing an important role in protein synthesis. To determine whether extracellular PDI mediates thrombus formation in an animal model, PDI expression, platelet accumulation, and fibrin generation were monitored in the blood vessels of mice by intravital fluorescence microscopy following laser-induced arteriolar injury. A time-dependent increase in PDI was observed in murine thrombi following injury. Infusion of the PDI inhibitor bacitracin or a blocking monoclonal antibody against PDI inhibited platelet thrombus formation and fibrin generation. Fibrin deposition is normal in mice lacking the G protein-coupled platelet receptor Par4, although there is no stable accumulation of platelets. Infusion of monoclonal antibodies against PDI into the circulation of Par4-/- mice prior to vessel wall injury inhibited fibrin generation. These results indicate that PDI is required in vivo in mice for both fibrin generation and platelet thrombus formation.논문정보
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