Phorbol ester-evoked Ca2+ signaling in human platelets is via autocrine activation of P(2X1) receptors, not a novel non-capacitative Ca2+ entry

M T Harper, Michael J Mason, Stewart O Sage, Alan G S Harper

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

15 Citations (Scopus)

Abstract

Platelets are reported to possess a protein kinase C (PKC)-dependent non-capacitative Ca(2+)entry (NCCE) pathway. The phorbol ester, phorbol, 12-myristate, 13-acetate (PMA) has been suggested to stimulate platelet NCCE. Recently we demonstrated important roles in store-operated Ca(2+)entry in human platelets for Na(+)/Ca(2+) exchangers (NCXs) and autocrine signaling between platelets after dense granule secretion. As PMA evokes dense granule secretion, we have investigated the role of NCXs and autocrine signaling in PMA-evoked Ca(2+)entry.
Original languageEnglish
Pages (from-to)1604-13
Number of pages10
JournalJournal of Thrombosis and Haemostasis
Volume8
Issue number7
DOIs
Publication statusPublished - Jul 2010

Keywords

  • Secretory Vesicles
  • Blood Platelets
  • Calcium
  • Humans
  • Receptors, Purinergic P2X1
  • Autocrine Communication
  • Adenosine Triphosphate
  • Phorbol Esters
  • Sodium-Calcium Exchanger
  • Calcium Signaling

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