Zink A, Scherübl H, Kliemann D, Höflich M, Ziegler R, Raue F
Abteilung Innere Medizin I, Universität Heidelberg, Germany.
Mol Cell Endocrinol. 1992 Aug;86(3):213-9. doi: 10.1016/0303-7207(92)90146-w.
The effect of somatostatin on cAMP accumulation and calcitonin secretion in C-cells of the rat medullary thyroid carcinoma cell line rMTC 6-23 was investigated. Intracellular cAMP accumulation as well as calcitonin secretion could be dose-dependently stimulated by rat growth hormone releasing factor (rGRF). The long-acting somatostatin analogue octreotide inhibited rGRF-stimulated cAMP accumulation and calcitonin secretion dose dependently but failed to block 8-bromo-cAMP-stimulated calcitonin secretion. The inhibitory effect of octreotide on rGRF-induced calcitonin secretion was partially abolished by pretreating the cells with pertussis toxin. The octreotide effect was not due to changes in the degradation of cAMP, as it was similarly seen in the presence of isobutylmethylxanthine. Thus we conclude that pertussis toxin-sensitive G-proteins are involved in the cAMP-mediated regulation of calcitonin secretion in C-cells.
研究了生长抑素对大鼠甲状腺髓样癌细胞系rMTC 6-23的C细胞中cAMP积累和降钙素分泌的影响。大鼠生长激素释放因子(rGRF)可剂量依赖性地刺激细胞内cAMP积累以及降钙素分泌。长效生长抑素类似物奥曲肽剂量依赖性地抑制rGRF刺激的cAMP积累和降钙素分泌,但未能阻断8-溴-cAMP刺激的降钙素分泌。用百日咳毒素预处理细胞可部分消除奥曲肽对rGRF诱导的降钙素分泌的抑制作用。奥曲肽的作用并非由于cAMP降解的变化,因为在异丁基甲基黄嘌呤存在的情况下也有类似现象。因此我们得出结论,百日咳毒素敏感的G蛋白参与了C细胞中cAMP介导的降钙素分泌调节。