Phospholipase Cgamma2 contributes to stable thrombus formation on VWF. FEBS Lett 2004 Aug 27;573(1-3):26-30
Date
08/26/2004Pubmed ID
15327970DOI
10.1016/j.febslet.2004.07.048Scopus ID
2-s2.0-4344564590 (requires institutional sign-in at Scopus site) 14 CitationsAbstract
Though phospholipase C PLCgamma2 is known to play an important role in platelet activation by collagen and fibrinogen, its importance in GPIb-mediated platelet activation is less well understood. To better understand the role of PLCgamma2 in GPIb-mediated adhesion and thrombus formation, we examined the ability of wild-type and PLCgamma2- deficient murine platelets to spread on immobilized von Willebrand factor (VWF) under static conditions, and to attach to and form thrombi on VWF under conditions of arterial shear. While absence of PLCgamma2 had only a minimal effect on platelet adhesion to immobilized VWF, its absence impaired spreading and profoundly affected thrombus growth and stability on VWF.
Author List
Rathore V, Wang D, Newman DK, Newman PJAuthors
Debra K. Newman PhD Investigator in the Blood Research Institute department at BloodCenter of WisconsinDebra K. Newman PhD Professor in the Pharmacology and Toxicology department at Medical College of Wisconsin
Demin Wang PhD Professor in the Microbiology and Immunology department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsBlood Platelets
Gene Deletion
Hemorheology
Mice
Phospholipase C gamma
Platelet Adhesiveness
Thrombosis
Type C Phospholipases
von Willebrand Factor
