Corticotropin releasing factor increases proopiomelanocortin messenger RNA in mouse anterior pituitary tumor cells.
Corticotropin releasing factor increases proopiomelanocortin messenger RNA in mouse anterior pituitary tumor cells.
复制标题
促肾上腺皮质激素释放因子增加小鼠垂体前叶肿瘤细胞中阿黑皮质素原信使 RNA。
DOI：
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发表时间：
1985
影响因子：
4.8
通讯作者：
T. Reisine
中科院分区：
文献类型：
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作者：
H. Affolter;T. Reisine
通过测定小鼠垂体前叶肿瘤细胞株（AtT-20/D16-16）中促肾上腺皮质激素（ACTH）的总细胞含量和阿黑皮素原（POMC）mRNA水平，评价了促肾上腺皮质激素释放因子（CRF）刺激促肾上腺皮质激素细胞合成ACTH的能力。CRF治疗引起的POMC mRNA水平的时间依赖性增加（使用杂交技术测量），以及在AtT-20细胞中的总ACTH含量升高。POMC mRNA水平的增加先于ACTH含量的变化，并在CRF停药后缓慢恢复至对照水平。CRF刺激后POMC mRNA水平的升高似乎是特异性的，因为β-肌动蛋白mRNA水平不受CRF治疗的影响。8-溴-cAMP和佛波酯均能增加AtT-20细胞中POMC mRNA的表达，提示CRF可能通过不同的蛋白激酶来调节POMC基因。CRF似乎激活POMC基因，因为用肽处理AtT-20细胞增加了细胞核中具有POMC基因转录物的预期分子量的RNA种类的水平。结果表明，促肾上腺皮质激素细胞持续暴露于CRF诱导这些细胞的ACTH合成能力的长期增加。
The ability of corticotropin releasing factor (CRF) to stimulate adrenocorticotropin (ACTH) synthesis in corticotrophs was assessed by measuring total cell content of ACTH and the levels of proopiomelanocortin (POMC) mRNA in a cloned tumor cell line of the mouse anterior pituitary (AtT-20/D16-16). CRF treatment caused a time-dependent increase in POMC mRNA levels (measured using a hybridization technique) as well as elevating total ACTH content in AtT-20 cells. The increase in POMC mRNA levels preceded changes in ACTH content and slowly returned toward control levels after CRF withdrawal. The rise in POMC mRNA levels following CRF stimulation appeared to be specific since beta-actin mRNA levels were not affected by CRF treatment. Both 8-bromo-cAMP and phorbol ester increased POMC mRNA levels in AtT-20 cells, suggesting that CRF may act through different protein kinases to regulate the POMC gene. CRF appears to activate the POMC gene since treatment of the AtT-20 cells with the peptide increased the levels of an RNA species in the nuclei having the expected molecular weight of the transcript of the POMC gene. The results indicate that continued exposure of corticotrophs to CRF induces long term increases in the ACTH synthetic capacity of those cells.