Pertussis toxin abolishes angiotensin II-induced phosphoinositide hydrolysis and prostaglandin synthesis in rat renal mesangial cells.
Pertussis toxin abolishes angiotensin II-induced phosphoinositide hydrolysis and prostaglandin synthesis in rat renal mesangial cells.
复制标题
百日咳毒素可消除大鼠肾系膜细胞中血管紧张素 II 诱导的磷酸肌醇水解和前列腺素合成。
作者：
J. Pfeilschifter;C. Bauer
用血管紧张素II（0.1 μ M）孵育大鼠肾系膜细胞，导致磷脂酰肌醇4，5-二磷酸的瞬时分解，二酰基甘油和磷脂酸的快速生成，45 Ca 2+内流增加，quin 2测定的细胞内[Ca 2 +]增加，前列腺素E2合成增加。所有这些过程都明显抑制时间和剂量依赖性事先暴露的细胞百日咳毒素。与此相反，离子载体A23187对45 Ca 2+内流和前列腺素E2合成的影响没有改变暴露的细胞百日咳毒素。毒素的作用与细胞内cAMP浓度的改变无关。用百日咳毒素孵育系膜细胞的膜部分导致Mr-42，000蛋白的ADP-核糖基化。从所有这些结果，这是可能的G蛋白参与受体介导的信号转导在肾系膜细胞。
Incubation of rat renal mesangial cells with angiotensin II (0.1 microM) resulted in transient breakdown of phosphatidylinositol 4,5-bisphosphate, rapid generation of diacylglycerol and phosphatidic acid, increased 45Ca2+ influx, increased intracellular [Ca2+] as measured by quin 2, and increased prostaglandin E2 synthesis. All of these processes were markedly inhibited time- and dose-dependently by prior exposure of cells to pertussis toxin. In contrast, the effects of the ionophore A23187 on 45Ca2+ influx and prostaglandin E2 synthesis were not altered by the exposure of the cells to pertussis toxin. The action of the toxin was not associated with alterations in cellular concentrations of cyclic AMP. Incubation of membrane fraction of mesangial cells with pertussis toxin resulted in ADP-ribosylation of Mr-42,000 protein. From all these results, it is likely that a G protein is involved in receptor-mediated signal transduction in renal mesangial cells.