Abstract
A rise in intracellular calcium concentration ([Ca 2+] i) is necessary for platelet activation. A major component of the [Ca 2+] i elevation occurs through store-operated Ca 2+ entry (SOCE). The aim of this study was to understand the contribution of the classical PKC isoform, PKCα to platelet SOCE, using platelets from PKCα-deficient mice. SOCE was reduced by approximately 50% in PKCα −/− platelets, or following treatment with bisindolylmaleimide I, a PKC inhibitor. However, TG-induced Mn 2+ entry was unaffected, which suggests that divalent cation entry through store-operated channels is not directly regulated. Blocking the autocrine action of secreted ADP or 5-HT on its receptors did not reproduce the effect of PKCα deficiency. In contrast, SN-6, a Na +/Ca 2+ exchanger inhibitor, did reduce SOCE to the same extent as loss of PKCα, as did replacing extracellular Na + with NMDG +. These treatments had no further effect in PKCα −/− platelets. These data suggest that PKCα enhances the extent of SOCE in mouse platelets by regulating Ca 2+ entry through the Na +/Ca 2+ exchanger.
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