Regulation of growth hormone-releasing hormone receptor messenger ribonucleic acid expression by glucocorticoids in MtT-S cells and in the pituitary gland of fetal rats.
Regulation of growth hormone-releasing hormone receptor messenger ribonucleic acid expression by glucocorticoids in MtT-S cells and in the pituitary gland of fetal rats.
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糖皮质激素对 MtT-S 细胞和胎鼠垂体中生长激素释放激素受体信使核糖核酸表达的调节。
作者：
H. Nogami;Kinji Inoue;H. Moriya;A. Ishida;S. Kobayashi;S. Hisano;M. Katayama;K. Kawamura
采用核糖核酸酶保护实验研究了胎鼠垂体和MtT-S克隆细胞中gh -释放激素受体（GHRH-R）信使RNA （mRNA）的表达调控。GHRH-R mRNA在胚胎日(E)19时首次检测到，此后迅速增加，在胚胎日(E) 21时达到最大值。用50 nM合成糖皮质激素地塞米松（dexamethasone， DEX）孵育E17或E18垂体，可诱导GHRH-R mRNA的表达，提示糖皮质激素在该mRNA的发育表达中起关键作用。在E19垂体中，dex24 h使GHRH-R mRNA增加60%，GH mRNA增加76%，但不影响pit-1 mRNA的表达，表明dex24 h对GH mRNA和GHRH-R mRNA的表达具有特异性。DEX对GHRH-R mRNA的积累具有时间依赖性，蛋白合成抑制剂puromycin （100 μ m）对GHRH-R mRNA的积累略有增强。在MtT-S细胞（从雌激素诱导的肿瘤中建立的垂体细胞系）中，DEX在2小时内以剂量依赖的方式诱导GHRH-R mRNA表达。嘌呤霉素（100微米）或环己亚胺（3.5微米）增强了这种诱导作用。而RNA合成抑制剂放线菌素D（1微米）在DEX或DEX +嘌呤霉素作用下均能完全抑制GHRH-R mRNA的积累，提示糖皮质激素主要通过刺激mRNA转录诱导GHRH-R mRNA。这些结果提示：大鼠胎儿垂体中GHRH-R mRNA的积累通常发生在E19，可能是由于糖皮质激素直接作用于垂体，刺激GHRH-R mRNA转录；糖皮质激素受体的表达是大鼠生长激素细胞发育过程中的一个重要事件。因此，免疫细胞化学结果表明，E17和E18之间未成熟GH细胞中的糖皮质激素受体增加。本研究结果也提示MtT-S细胞可能是进一步研究GHRH-R基因表达调控分子机制的良好模型。
Regulation of GH-releasing hormone receptor (GHRH-R) messenger RNA (mRNA) expression was studied, with the ribonuclease protection assay, in the fetal rat pituitary gland and in MtT-S clonal cells. GHRH-R mRNA was first detected on embryonic day (E)19 and increased rapidly thereafter, to reach a maximum at E21. Incubation of E17 or E18 pituitaries with 50 nM dexamethasone (DEX), a synthetic glucocorticoid, induced GHRH-R mRNA expression, suggesting that glucocorticoids play a pivotal role in the developmental expression of this mRNA. In E19 pituitaries, 24 h treatment with DEX increased GHRH-R mRNA by 60%, and GH mRNA by 76%, but did not affect pit-1 mRNA level, suggesting that the effect of DEX is specific for expressions of GH mRNA and GHRH-R mRNA. The accumulation of GHRH-R mRNA by DEX was time dependent, and it was slightly enhanced by the protein synthesis inhibitor, puromycin (100 microM). In MtT-S cells (a pituitary cell line established from an estrogen-induced tumor), DEX induced GHRH-R mRNA expression within 2 h in a dose-dependent manner. This induction was augmented by puromycin (100 microM) or cycloheximide (3.5 microM). However, the RNA synthesis inhibitor Actinomycin D (1 microM) completely inhibited GHRH-R mRNA accumulation in response to either DEX or DEX plus puromycin, suggesting that glucocorticoids induce GHRH-R mRNA mainly through stimulation of mRNA transcription. These results suggest: that GHRH-R mRNA accumulation in the fetal pituitary gland of rats normally occurs at E19, probably because of the direct action of glucocorticoids on the pituitary gland, to stimulate GHRH-R mRNA transcription; and that the expression of glucocorticoid receptors is an important event in GH cell development in rats. Accordingly, immunocytochemical results suggest an increase in glucocorticoid receptors in immature GH cells between E17 and E18. The present results also imply that MtT-S cells may be a good model in which to further study the molecular mechanisms of the regulation of GHRH-R gene expression.
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生长激素释放因子（GRF）调节其自身受体的表达。
DOI：
10.1210/endo.137.6.8641220
发表时间：
1996
期刊：
Endocrinology.
影响因子：
--
作者：
Horikawa,R;Hellmann,P;Cella,SG;Torsello,A;Day,RN;Muller,EE;Thorner,MO
通讯作者：
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影响因子：
4.1
作者：
Ishikawa,K;Katakami,H;Jansson,JO;Frohman,LA
通讯作者：
Frohman,LA
大鼠垂体前叶膜匀浆中的生长激素释放因子结合位点：糖皮质激素的调节。
影响因子：
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作者：
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通讯作者：
Vale,W
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影响因子：
4.8
作者：
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通讯作者：
Boockfor,FR
生长激素释放激素受体信使核糖核酸水平的同源下调。
DOI：
10.1210/endo.138.3.5029
发表时间：
1997
期刊：
Endocrinology.
影响因子：
--
作者：
Aleppo,G;Moskal2nd,SF;DeGrandis,PA;Kineman,RD;Frohman,LA
通讯作者：
Frohman,LA