Thrombin-induced release of von Willebrand factor from endothelial cells is mediated by phospholipid methylation. Prostacyclin synthesis is independent of phospholipid methylation.

摘要: The biochemical events that lead to thrombin-stimulated release of von Willebrand factor and prostacyclin synthesis in cultured endothelial cells are examined. Treatment human umbilical vein with thrombin results an instantaneous increase phospholipid methylation which can be blocked by 3-deazaadenosine, a methyltransferase inhibitor. 3-Deazaadenosine also blocks the thrombin-induced Ca2+ influx into factor, indicating these processes coupled. phorbol ester 4 beta-phorbol 12-myristate 13-acetate (PMA) ionophore A23187 both bypass directly stimulate release. In contrast stimulus-induced release, cannot 3-deazaadenosine. Similarly, incubation EDTA has no influence on synthesis, PMA stimulatory effect synthesis. These observations indicate induces different metabolic responses cells: followed influx, subsequently leads liberation arachidonic acid from phospholipids for formation, is independent influx.