Remy-Jouet I, Delarue C, Feuilloley M, Vaudry H
European Institute for Peptide Research, Laboratory of Cellular and Molecular Neuroendocrinology, INSERM 4413, UA CNRS, University of Rouen, Mont-Saint-Aignan, France.
J Steroid Biochem Mol Biol. 1994 Jul;50(1-2):55-9. doi: 10.1016/0960-0760(94)90172-4.
In a previous report, we have shown that endothelin-1 (ET-1) is a potent stimulator of corticosterone and aldosterone secretion by frog adrenocortical cells. In the present study, we examine the possible involvement of cytoskeletal elements in the mechanism of action of ET-1 on corticosteroid secretion from frog adrenal gland. The microfilament disrupting agent cytochalasin B (5 x 10(-5) M) induced a reversible inhibition of the spontaneous secretion of corticosteroid and blocked the response of adrenocortical cells to ET-1 (5 x 10(-9) M). In contrast, the antimicrotubular agent vinblastine (10(-5) M) and the intermediate filament inhibitor beta-beta' iminodipropionitrile (10(-3) M) had virtually no effect on both spontaneous and endothelin-induced steroidogenesis. Taken together, these results indicate that, in the frog adrenal gland, the integrity of the microfilament network is required for the corticotropic activity of ET-1 whereas microtubules and intermediate filaments are apparently not involved in the mechanism of action of ET-1.
在之前的一份报告中,我们已经表明内皮素-1(ET-1)是青蛙肾上腺皮质细胞分泌皮质酮和醛固酮的有效刺激物。在本研究中,我们研究了细胞骨架成分是否可能参与ET-1对青蛙肾上腺皮质类固醇分泌的作用机制。微丝破坏剂细胞松弛素B(5×10⁻⁵ M)可诱导可逆性抑制皮质类固醇的自发分泌,并阻断肾上腺皮质细胞对ET-1(5×10⁻⁹ M)的反应。相比之下,抗微管剂长春碱(10⁻⁵ M)和中间丝抑制剂β-β'亚氨基二丙腈(10⁻³ M)对自发和内皮素诱导的类固醇生成几乎没有影响。综上所述,这些结果表明,在青蛙肾上腺中,ET-1的促肾上腺皮质激素活性需要微丝网络的完整性,而微管和中间丝显然不参与ET-1的作用机制。