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细胞骨架在青蛙肾上腺对血管紧张素II、乙酰胆碱和血清素的类固醇生成反应中的作用。

Involvement of the cytoskeleton in the steroidogenic response of frog adrenal glands to angiotensin II, acetylcholine and serotonin.

作者信息

Feuilloley M, Netchitaïlo P, Delarue C, Leboulenger F, Benyamina M, Pelletier G, Vaudry H

机构信息

UA CNRS 650, Unité Alliée à l'INSERM, Faculté des Sciences, Université de Rouen BP, Mont-Saint-Aignan, France.

出版信息

J Endocrinol. 1988 Sep;118(3):365-74. doi: 10.1677/joe.0.1180365.

Abstract

In order to determine the role of the cytoskeleton in adrenal steroidogenesis, we have studied the effect of cytochalasin B (a microfilament-disrupting agent) and vinblastine (an antimicrotubular drug) on corticosteroid secretion by frog interrenal tissue in vitro. Perifusion of interrenal fragments with cytochalasin B (50 mumol/l) induced a marked inhibition of basal corticosteroid output. In addition, stimulation of corticosteroidogenesis by all corticotrophic factors was also inhibited by cytochalasin B. Using an immunohistochemical technique and specific anti-tubulin antiserum, we verified that vinblastine (10 mumol/l) was responsible for the disappearance of the microtubular network in adrenocortical cells. Administration of vinblastine (10 mumol/l) did not affect the spontaneous secretion of corticosterone and aldosterone and had no effect on the steroidogenic response of interrenal glands to angiotensin II and acetylcholine. In contrast, vinblastine was responsible for a marked decrease in serotonin-induced stimulation of corticosteroid production. On the other hand, data from high-performance liquid chromatography showed that infusion of cytochalasin B or vinblastine was not associated with the production of any new steroid which could interfere in the radioimmunoassays. Taken together, these data suggest that microfilaments are involved in a late and common step of corticosteroidogenesis while microtubules are only required for the coupling of the secretory response to certain corticotrophic factors such as ACTH and serotonin.

摘要

为了确定细胞骨架在肾上腺类固醇生成中的作用,我们研究了细胞松弛素B(一种破坏微丝的药物)和长春花碱(一种抗微管药物)对青蛙肾间组织体外皮质类固醇分泌的影响。用细胞松弛素B(50 μmol/l)对肾间组织碎片进行灌流可显著抑制基础皮质类固醇的分泌。此外,细胞松弛素B还抑制了所有促肾上腺皮质激素因子对类固醇生成的刺激作用。我们使用免疫组织化学技术和特异性抗微管蛋白抗血清,证实长春花碱(10 μmol/l)导致肾上腺皮质细胞微管网络消失。给予长春花碱(10 μmol/l)不影响皮质酮和醛固酮的自发分泌,对肾间腺对血管紧张素II和乙酰胆碱的类固醇生成反应也无影响。相反,长春花碱导致血清素诱导的皮质类固醇生成刺激作用显著降低。另一方面,高效液相色谱数据显示,灌注细胞松弛素B或长春花碱与任何可能干扰放射免疫测定的新类固醇的产生无关。综上所述,这些数据表明微丝参与了皮质类固醇生成的一个晚期共同步骤,而微管仅在分泌反应与某些促肾上腺皮质激素因子(如促肾上腺皮质激素和血清素)偶联时才是必需的。

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