Mechanism of thrombin-induced rise in platelet fructose 2,6-bisphosphate content. Studies using phorbol myristate acetate, dioctanoylglycerol and ionophore A23187

Biochem J. 1987 Jun 15;244(3):547-51. doi: 10.1042/bj2440547.

Abstract

The mechanism by which thrombin increases platelet fructose 2,6-bisphosphate content was investigated. The action of thrombin was mimicked by phorbol 12 myristate 13-acetate and 1,2-dioctanoylglycerol. Ca2+ with A23187 potentiated the action of both these compounds. The action of thrombin required mobilization of intracellular and extracellular Ca2+ and was not decreased by indomethacin. This study suggests that protein kinase C activation and Ca2+ mobilization are both involved in the activation of glycolysis by thrombin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blood Platelets / drug effects
  • Blood Platelets / metabolism*
  • Calcimycin / pharmacology
  • Calcium / pharmacology
  • Diglycerides / pharmacology
  • Egtazic Acid / pharmacology
  • Fructosediphosphates / blood*
  • Glycolysis / drug effects
  • Hexosediphosphates / blood*
  • Humans
  • Indomethacin / pharmacology
  • Tetradecanoylphorbol Acetate / pharmacology
  • Thrombin / pharmacology*

Substances

  • Diglycerides
  • Fructosediphosphates
  • Hexosediphosphates
  • 1,2-dioctanoylglycerol
  • Calcimycin
  • Egtazic Acid
  • fructose 2,6-diphosphate
  • Thrombin
  • Tetradecanoylphorbol Acetate
  • Calcium
  • Indomethacin