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Characterisation of Rac activation in thrombin‐ and collagen‐stimulated human blood platelets
Author(s) -
Soulet Carine,
Gendreau Sandra,
Missy Karine,
Benard Valérie,
Plantavid Monique,
Payrastre Bernard
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)02984-2
Subject(s) - heterotrimeric g protein , platelet activation , thrombin , microbiology and biotechnology , chemistry , phospholipase c , cdc42 , phospholipase d , integrin , g protein , rac gtp binding proteins , protein kinase c , platelet , rac1 , gtpase , kinase , signal transduction , biochemistry , receptor , biology , immunology
In this study, we characterised the mechanisms of Rac GTPase activation in human platelets stimulated by two physiological agonists, either thrombin, acting through membrane receptors coupled to heterotrimeric G‐proteins, or collagen which is known to mobilise a tyrosine kinase‐dependent pathway. Both agonists induced a rapid activation of Rac that was not significantly affected by the inhibition of integrin α IIb β 3 engagement. Using pharmacological inhibitors, we found that phospholipase C activation and calcium mobilisation were essential for platelet Rac activation by either thrombin or collagen whereas protein kinase C inhibition was without effect. In contrast to Rac, Cdc42 activation was independent of phospholipase C activation, indicating that the two GTPases are differently regulated. We also found that phosphoinositide 3‐kinase was not required for Rac activation in response to thrombin but was involved in its activation by collagen.