Regulation of bradykinin receptor level by cholera toxin, pertussis toxin and forskolin in cultured human fibroblasts.
Regulation of bradykinin receptor level by cholera toxin, pertussis toxin and forskolin in cultured human fibroblasts.
复制标题
霍乱毒素、百日咳毒素和毛喉素对培养的人成纤维细胞中缓激肽受体水平的调节。
DOI：
10.1111/j.1476-5381.1991.tb09791.x
复制
发表时间：
1991
影响因子：
7.3
通讯作者：
Villereal,ML
中科院分区：
文献类型：
--
作者：
Etscheid,BG;Ko,PH;Villereal,ML
1. 在预先标记[3H]-花生四烯酸的无血清人包皮（HSWP）成纤维细胞中，研究了细菌毒素对缓激肽触发的花生四烯酸释放的影响。将HSWP细胞暴露于霍乱毒素、百日咳毒素或福斯克林中18小时，可增强缓激肽刺激的花生四烯酸和代谢物的释放。2. 用这些药物长期处理HSWP细胞也导致细胞表面[3H]-缓激肽结合增加3至4倍。与环己亚胺或放线菌素d同时孵育可抑制这种升高。此外，霍乱毒素和foreskolin在野生型PC12细胞中增加了[3H]-缓激肽的结合，而在环amp依赖性蛋白激酶II型活性降低的突变型PC12细胞中则没有。3. 由此可见，霍乱毒素、百日咳毒素和福斯可林对缓激肽的作用增强了花生四烯酸的释放，增加了HSWP成纤维细胞中缓激肽受体的数量。一种循环amp依赖机制似乎介导了毒素和福斯克林的作用。
1. The effect of bacterial toxins on bradykinin-triggered release of arachidonic acid was studied in serum-deprived human foreskin (HSWP) fibroblasts prelabelled with [3H]-arachidonic acid. An 18-h exposure of HSWP cells to cholera toxin, pertussis toxin, or forskolin enhanced the bradykinin-stimulated release of arachidonic acid and metabolites. 2. Prolonged treatment of HSWP cells with these agents also caused a 3 to 4 fold rise in cell surface [3H]-bradykinin binding. The rise was inhibited by concurrent incubation with cycloheximide or actinomycin D. In addition, cholera toxin and foreskolin increased [3H]-bradykinin binding in wildtype PC12 cells, but not in mutant PC12 cells with reduced cyclic AMP-dependent protein kinase type II activity. 3. In conclusion, cholera toxin, pertussis toxin and forskolin enhanced arachidonic acid release in response to bradykinin, and increased the number of bradykinin receptors in HSWP fibroblasts. A cyclic AMP-dependent mechanism appears to mediate the actions of the toxins and forskolin.