霍乱毒素、百日咳毒素和福斯高林对培养的人成纤维细胞中缓激肽受体水平的调节
Regulation of bradykinin receptor level by cholera toxin, pertussis toxin and forskolin in cultured human fibroblasts.
作者信息
Etscheid B G, Ko P H, Villereal M L
机构信息
Department of Pharmacological and Physiological Sciences, University of Chicago, IL 60637.
出版信息
Br J Pharmacol. 1991 Jun;103(2):1347-50. doi: 10.1111/j.1476-5381.1991.tb09791.x.
Abstract
- 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.
摘要
- 在预先用[3H]-花生四烯酸标记的血清饥饿的人包皮（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、百日咳毒素或福斯高林18小时，可增强缓激肽刺激的花生四烯酸及其代谢产物的释放。2. 用这些试剂对HSWP细胞进行长时间处理，还会导致细胞表面[3H]-缓激肽结合增加3至4倍。同时与环己酰亚胺或放线菌素D孵育可抑制这种增加。此外，霍乱毒素和福斯高林可增加野生型PC12细胞中[3H]-缓激肽的结合，但在II型环磷酸腺苷依赖性蛋白激酶活性降低的突变型PC12细胞中则不会。3. 总之，霍乱毒素、百日咳毒素和福斯高林可增强缓激肽诱导的花生四烯酸释放，并增加HSWP成纤维细胞中缓激肽受体的数量。一种环磷酸腺苷依赖性机制似乎介导了毒素和福斯高林的作用。
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