Protein kinase C translocation in human blood platelets

Life Sci. 1990;47(16):1419-25. doi: 10.1016/0024-3205(90)90520-2.


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 microM concentrations did not induce redistribution of platelet PKC. Serotonin (0.5-100 microM) and the specific 5-HT2 receptor agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) (10-100 microM) but not the 5-HT1A or 5-HT1B 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-HT2 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-HT2 receptors.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Blood Platelets / drug effects
  • Blood Platelets / enzymology*
  • Cell Membrane / enzymology
  • Cytosol / enzymology
  • Humans
  • In Vitro Techniques
  • Ketanserin / pharmacology
  • Kinetics
  • Protein Kinase C / blood*
  • Serotonin / pharmacology*
  • Tetradecanoylphorbol Acetate / pharmacology*
  • Thrombin / pharmacology*


  • Serotonin
  • Ketanserin
  • Protein Kinase C
  • Thrombin
  • Tetradecanoylphorbol Acetate