Nolte C, Eigenthaler M, Schanzenbächer P, Walter U
Medizinische Universitätsklinik, Klinische Forschergruppe, Würzburg, Federal Republic of Germany.
J Biol Chem. 1991 Aug 5;266(22):14808-12.
We reported previously that a 46/50-kDa membrane-associated vasodilator-stimulated phosphoprotein (VASP) is phosphorylated in intact human platelets in response to both cGMP- and cAMP-elevating vasodilator drugs and presented evidence that this is mediated by cGMP- and cAMP-dependent protein kinases, respectively. VASP was recently purified and an antibody against it was developed which detects a phosphorylation-induced mobility change of VASP in sodium dodecyl sulfate-polyacrylamide gel electrophoresis (Halbrügge, M., Friedrich, C., Eigenthaler, M., Schanzenbächer, P., and Walter, U. (1990) J. Biol. Chem. 265, 3088-3093). We have now used these methods for the quantitative analysis of VASP phosphorylation during coincubations of human endothelial cells and human platelets. Endothelial cell-derived factors caused the rapid, stoichiometric, and reversible phosphorylation of platelet VASP during these coincubations. Other experiments indicated that the endothelium-derived factors which stimulate VASP phosphorylation are prostacyclin and endothelium-derived relaxing factor whose effects are mediated by cAMP/cAMP-dependent protein kinase and cGMP/cGMP-dependent protein kinase, respectively. The results suggest that VASP phosphorylation is an important component of the inhibitory effects of prostacyclin and endothelium-derived relaxing factor on platelet activation and that VASP phosphorylation is a useful biochemical marker for the interaction of endothelial cells and platelets.
我们先前报道,一种46/50-kDa膜相关的血管舒张刺激磷蛋白(VASP)在完整的人血小板中会因能升高cGMP和cAMP的血管舒张药物而发生磷酸化,并提出证据表明这分别是由cGMP依赖性蛋白激酶和cAMP依赖性蛋白激酶介导的。VASP最近已被纯化,并开发了一种针对它的抗体,该抗体可在十二烷基硫酸钠-聚丙烯酰胺凝胶电泳中检测到VASP磷酸化诱导的迁移率变化(哈尔布鲁格,M.,弗里德里希,C.,艾根塔勒,M.,尚岑贝彻,P.,和瓦尔特,U.(1990年)《生物化学杂志》265,3088 - 3093)。我们现在已使用这些方法对人内皮细胞与人血小板共孵育期间VASP磷酸化进行定量分析。在这些共孵育过程中,内皮细胞衍生因子导致血小板VASP快速、化学计量且可逆的磷酸化。其他实验表明,刺激VASP磷酸化的内皮细胞衍生因子是前列环素和内皮细胞衍生舒张因子,其作用分别由cAMP/cAMP依赖性蛋白激酶和cGMP/cGMP依赖性蛋白激酶介导。结果表明,VASP磷酸化是前列环素和内皮细胞衍生舒张因子对血小板活化抑制作用的重要组成部分,并且VASP磷酸化是内皮细胞与血小板相互作用的一种有用的生化标志物。