Schalkwijk C, Vervoordeldonk M, Pfeilschifter J, Märki F, van den Bosch H
Centre for Biomembranes and Lipid Enzymology, Utrecht, The Netherlands.
Biochem Biophys Res Commun. 1991 Oct 15;180(1):46-52. doi: 10.1016/s0006-291x(05)81252-5.
We have previously described that treatment of rat glomerular mesangial cells with interleukin-1 beta, tumor necrosis factor or forskolin stimulates the synthesis and secretion of prostaglandin E2 and group II phospholipase A2. We now report that pretreatment of the mesangial cells with dexamethasone dose-dependently suppresses the cytokines- and forskolin-induced synthesis of prostaglandin E2 as well as the induced synthesis and secretion of group II phospholipase A2. These observations implicate that the inhibition of the cellular or secreted phospholipase A2 activity by dexamethasone in rat mesangial cells is not due to induced synthesis of phospholipase A2 inhibitory proteins but caused by direct inhibition of phospholipase A2 protein expression.
我们之前曾描述过,用白细胞介素-1β、肿瘤坏死因子或福斯高林处理大鼠肾小球系膜细胞会刺激前列腺素E2和II型磷脂酶A2的合成与分泌。我们现在报告,用地塞米松对系膜细胞进行预处理会剂量依赖性地抑制细胞因子和福斯高林诱导的前列腺素E2合成以及II型磷脂酶A2的诱导合成与分泌。这些观察结果表明,地塞米松对大鼠系膜细胞中细胞型或分泌型磷脂酶A2活性的抑制不是由于诱导合成磷脂酶A2抑制蛋白,而是由直接抑制磷脂酶A2蛋白表达所致。