Hussa R O
In Vitro. 1979 Apr;15(4):237-45. doi: 10.1007/BF02618946.
The BeWo trophoblastic cell line was employed to assess the requirement for microtubules and cellular energy in human chorionic gonadotropin (hCG) secretion. In contrast to the general inhibitory effect of colchicine and vincristine on hormone secretion in systems involving exocytosis, wide concentration ranges of these antimicrotubule agents caused enhancement of hCG secretion. Similarly, cytochalasin B, an agent that interferes with microfilament function, doubled both basal hCG secretion, and secretion of hCG stimulated by 1 mM dibutyryl cyclic AMP plus 1 mM theophylline (dbT). Inhibitors of cellular energy production (2,4-dinitrophenol, malonate, azide) decreased both secreted and cellular levels of hormone. High concentrations of K+ gave no enhancement of basal or dbT-stimulated hCG secretion, nor any reduction of cellular hCG levels. These findings contrasted with observations of others in secretory systems involving exocytosis, in which high K+ potentiated basal or stimulated hormone release and depleted cellular stores of hormone. It was concluded that the process of hCG secretion in the malignant trophoblast is fundamentally different from the mechanism of protein hormone secretion in other tissues.
采用BeWo滋养层细胞系来评估人绒毛膜促性腺激素(hCG)分泌过程中对微管和细胞能量的需求。与秋水仙碱和长春新碱在涉及胞吐作用的系统中对激素分泌的普遍抑制作用相反,这些抗微管药物在很宽的浓度范围内都能促进hCG的分泌。同样,细胞松弛素B是一种干扰微丝功能的药物,它能使基础hCG分泌以及由1 mM二丁酰环磷腺苷(dbT)加1 mM氨茶碱刺激后的hCG分泌增加一倍。细胞能量产生的抑制剂(2,4-二硝基苯酚、丙二酸、叠氮化物)降低了激素的分泌水平和细胞内激素水平。高浓度的K+既没有增强基础的或dbT刺激的hCG分泌,也没有降低细胞内hCG水平。这些发现与其他涉及胞吐作用的分泌系统中的观察结果形成对比,在那些系统中,高K+能增强基础的或刺激后的激素释放,并耗尽细胞内的激素储存。得出的结论是,恶性滋养层细胞中hCG的分泌过程与其他组织中蛋白质激素的分泌机制有根本的不同。