Protein kinase C alpha enhances sodium-calcium exchange during store-operated calcium entry in mouse platelets

MT Harper, JD. Molkentin, AW Poole

Research output: Contribution to journalArticle (Academic Journal)peer-review

12 Citations (Scopus)

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.
Translated title of the contributionProtein kinase C alpha enhances sodium-calcium exchange during store-operated calcium entry in mouse platelets
Original languageEnglish
Pages (from-to)333 - 340
JournalCell Calcium
Volume48(6)
Publication statusPublished - Dec 2010

Bibliographical note

Author of Publication Reviewed: Harper MT, Molkentin JD, Poole AW

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