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  • Title: Effect of clopidogrel treatment on ADP-induced phosphorylations in rat platelets.
    Author: Savi P, Artçanuthurry V, Bornia J, Grelac F, Maclouf J, Levy-Toledano S, Herbert JM.
    Journal: Br J Haematol; 1997 Apr; 97(1):185-91. PubMed ID: 9136964.
    Abstract:
    Phosphorylations induced by 2-MeS-ADP, a potent agonist of platelet ADP receptors, have been studied in rat platelets, and the effect of clopidogrel, a compound which inhibits platelet aggregation by selectively reducing the binding of ADP to its low affinity receptors on platelets, has been determined. 2-MeS-ADP induced platelet activation (shape change and aggregation) simultaneously with the phosphorylation of myosin light chain (P20) and plekstrin (P47). Phosphorylation of P20 and P47 was transient, a maximum being observed 10 s after addition of the agonist when shape change reached its maximum. P20 and P47 phosphorylations were not strongly affected by clopidogrel treatment. Following stimulation of platelets with 2-MeS-ADP, several proteins were phosphorylated at tyrosine residues. Clopidogrel treatment inhibited the increase in phosphorylation of P140, P100, P80/85, P66 and P55 concomitantly with the inhibition of platelet aggregation. However, clopidogrel did not interfere with the early phosphorylation of the P80/85 kD doublet which occurs at the time of the shape change. P80/85, identified by immunodetection as cortactin, could be involved in the reorganization of the cytoskeleton necessary for morphological changes. Thus, by using clopidogrel-treated rat platelets, we were able to determine some of the phosphorylations coupled either to clopidogrel-resistant high-affinity ADP receptors leading to shape change or to clopidogrel sensitive low-affinity ADP receptors coupled to the aggregation process.
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