Leszczynski D, Ustinov J
Fourth Department of Surgery, University of Helsinki, Finland.
FEBS Lett. 1990 Apr 9;263(1):117-20. doi: 10.1016/0014-5793(90)80718-x.
Prostacyclin is generated by cultured rat endothelial cells. Compound blocking activity of protein kinase C and cyclic nucleotide-dependent protein kinases (H7) and compound blocking interaction between Ca2+ and calmodulin (W7) diminish generation of prostacyclin in rat endothelial cells. These compounds give a synergistic effect when they are introduced to the endothelial cell cultures simultaneously. Compound HA1004, an inhibitor of cAMP- and cGMP-dependent protein kinases has no effect on prostacyclin generation. Lipoxin A4, a potent direct stimulator of protein kinase C, rapidly induces prostacyclin generation in rat endothelium in a dose- and time-dependent fashion. Lipoxin A4-induced generation of prostacyclin can be inhibited by H7 and W7 but not by HA1004. Lipoxin B4 has no significant effect on prostacyclin generation in rat endothelium. In conclusion, our results demonstrate that generation of prostacyclin by rat endothelial cells is regulated via a pathway involving protein kinase C and Ca2+.
前列环素由培养的大鼠内皮细胞产生。蛋白激酶C和环核苷酸依赖性蛋白激酶的化合物阻断活性（H7）以及钙（Ca2+）与钙调蛋白之间的化合物阻断相互作用（W7）会减少大鼠内皮细胞中前列环素的产生。当这些化合物同时引入内皮细胞培养物时，它们会产生协同作用。化合物HA1004是一种环磷酸腺苷（cAMP）和环磷酸鸟苷（cGMP）依赖性蛋白激酶的抑制剂，对前列环素的产生没有影响。脂氧素A4是蛋白激酶C的一种强效直接刺激剂，能以剂量和时间依赖性方式迅速诱导大鼠内皮细胞产生前列环素。H7和W7可抑制脂氧素A4诱导的前列环素产生，但HA1004不能。脂氧素B4对大鼠内皮细胞中前列环素的产生没有显著影响。总之，我们的结果表明，大鼠内皮细胞产生前列环素是通过一条涉及蛋白激酶C和钙的途径来调节的。
