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Protein kinase C translocation in human blood platelets
Journal article   Peer reviewed

Protein kinase C translocation in human blood platelets

Hoau-Yan Wang and Eitan Friedman
Life sciences (1973), v 47(16), pp 1419-1425
1990
PMID: 2250559

Abstract

Protein kinase C (PKC) activity and translocation in response to the phorbol ester, phorbol 12-myristate, 13-acetate (PMA), serotonin (5-HT) and thrombin was assessed in human platelets. Stimulation with PMA and 5-HT for 10 minutes or thrombin for 1 minute elicited platelet PKC translocation from cytosol to membrane. The catecholamines, norepinephrine or epinephrine at 10 μM concentrations did not induce redistribution of platelet PKC. Serotonin (0.5–100 μM) and the specific 5-HT 2 receptor agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) (10–100 μM) but not the 5-HT 1A or 5-HT 1B agonists, (±) 8-hydroxy-dipropylamino-tetralin (8-OH-DPAT) or 5-methoxy-3-3- (1,2,3,6-tetrahydro-4-pyridin) 1H-indole succinate (RU 24969) induced dose-dependent PKC translocations. Serotonin-evoked PKC translocation was blocked by selective 5-HT 2 receptor antagonists, ketanserin and spiroperidol. These results suggest that, in human platelets, PMA, thrombin and 5-HT can elicit PKC translocation from cytosol to membrane. Serotonin-induced PKC translocation in platelets is mediated via 5-HT 2 receptors.

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Medicine, Research & Experimental
Pharmacology & Pharmacy
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