Thromb Haemost 1996; 76(02): 248-252
DOI: 10.1055/s-0038-1650563
Original Article
Schattauer GmbH Stuttgart

lonomycin-stimulated Arachidonic Acid Release in Human Platelets: a Role for Protein Kinase C and Tyrosine Phosphorylation

Philip G Hargreaves
1   The Department of Biochemistry, Cambridge, UK
,
Susanne Jenner
2   Physiological Laboratory, University of Cambridge, Cambridge, UK
,
Janet E Merritt
3   Roche Research Centre, Welwyn Garden City, Herts, UK
,
Stewart O Sage
2   Physiological Laboratory, University of Cambridge, Cambridge, UK
,
Richard W Farndale
1   The Department of Biochemistry, Cambridge, UK
› Author Affiliations
Further Information

Publication History

Received 13 December 1995

Accepted after resubmission 17 April 1996

Publication Date:
10 July 2018 (online)

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Summary

Collagen (10-90 Μg/ml) and ionomycin (1 ΜM; a calcium iono-phore) each evoked rises in intracellular free calcium, protein kinase C activity and arachidonic acid release in human platelets, and as previously demonstrated for collagen, ionomycin (1 p,M) stimulated protein tyrosine phosphorylation. However, at lower concentrations (60 and 250 nM) ionomycin selectively mobilised calcium. Ro31-8220 (a selective inhibitor of protein kinase C) inhibited (by 50%) ionomycin-stimulated arachidonic acid release. Genistein (an inhibitor of protein tyrosine kinases) also reduced by 50% ionomycin-stimulated arachidonic acid release. In combination, genistein and Ro31-8220 abolished ionomycin-stimulated arachidonic acid release. These findings show 1) that a rise in calcium is not sufficient, and 2) the activation of both protein kinase C and protein tyrosine phosphorylation is necessary, for full ionomycin-stimulated arachidonic acid release in human platelets.