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首页> 外文期刊>Journal of the Society for Gynecologic Investigation >Ontogeny and effects of thyroid hormone on beta1-adrenergic receptor mRNA expression in ovine fetal kidney cortex.
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Ontogeny and effects of thyroid hormone on beta1-adrenergic receptor mRNA expression in ovine fetal kidney cortex.

机译：绵羊胎肾皮质的个体发育及甲状腺激素对β1-肾上腺素能受体mRNA表达的影响。

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OBJECTIVE: Previous studies indicate that thyroidectomy (TX) decreases renin gene expression in ovine fetal renal cortex in late gestation. Fetal ovine renin-containing renocortical cells become increasingly responsive to beta-adrenergic stimulation as gestation proceeds. Increases in plasma thyroid hormone concentrations parallel this change, suggesting that there is a positive developmental relationship between the two. To examine this hypothesis, we determined the ontogeny of beta1-adrenergic receptor (beta1R) mRNA expression, and the effect of thyroid hormone on in vivo and in vitro expression in fetal sheep. METHODS: Renocortical tissue was obtained from naive, TX, and sham-operated fetuses to determine beta1R mRNA levels. Renin-containing renocortical cells from TX or sham fetuses were treated with isoproterenol (Iso) or forskolin (FSK) for analysis of cellular cyclic adenosine monophosphate (cAMP) levels. Renocortical cells from naive fetuses were treated with triiodothyronine (T3) to assess cellular beta1R mRNA levels. Fetal plasma thyroxine (T4) level was determined. RESULTS: Renocortical beta1R mRNA expression increased significantly between 100 and 140 days' gestational age (dGA), while TX attenuated this increase (P <.01). Renocortical cellular cAMP levels were higher in sham compared to TX fetuses following incubation with Iso or FSK (P <.05). Cells incubated with T3 exhibited significantly increased beta1R mRNA expression (P <.05). CONCLUSION: The data suggest that thyroid hormone may be involved in modulating ovine fetal renocortical beta1R gene expression during development. We speculate that the increased beta1R mRNA expression in renal cortical cells as development progresses may mediate the increases in renin gene response to beta-adrenergic stimulation in late gestation.
机译：目的：先前的研究表明，在妊娠晚期，甲状腺切除术（TX）会降低绵羊胎儿肾皮质的肾素基因表达。随着妊娠的进行，胎儿的含肾素肾上腺皮质细胞对β-肾上腺素刺激的反应越来越强。血浆甲状腺激素浓度的增加与此变化平行，这表明两者之间存在正向发育关系。为了检验这一假设，我们确定了β1-肾上腺素能受体（beta1R）mRNA的表达，以及甲状腺激素对胎羊体内和体外表达的影响。方法：从幼稚，得克萨斯州和假手术的胎儿获得肾皮质组织，以确定β1RmRNA水平。用异丙肾上腺素（Iso）或福斯高林（FSK）处理来自TX或假胎儿的含肾素的肾上腺皮质细胞，以分析细胞环一磷酸腺苷（cAMP）的水平。原始胎儿的肾皮质细胞用三碘甲状腺素（T3）处理，以评估细胞beta1R mRNA水平。确定胎儿血浆甲状腺素（T4）水平。结果：在100至140天的胎龄（dGA）之间，肾皮质β1RmRNA表达显着增加，而TX减弱了这种增加（P <.01）。与Iso或FSK孵育后，伪造血的肾皮质细胞cAMP水平高于TX胎儿（P <.05）。用T3孵育的细胞显示出beta1R mRNA表达显着增加（P <.05）。结论：数据提示甲状腺激素可能参与发育过程中调节绵羊胎儿肾皮质β1R基因的表达。我们推测随着发育的进展，肾皮质细胞中beta1R mRNA表达的增加可能会介导妊娠后期对β-肾上腺素能刺激的肾素基因应答的增加。

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