Estrogen Receptor Alpha Regulates Retinaldehyde Dehydrogenase 1 Expression in Rat Anterior Pituitary Cells
Estrogen Receptor Alpha Regulates Retinaldehyde Dehydrogenase 1 Expression in Rat Anterior Pituitary Cells
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DOI：
10.1507/endocrj.k09e-115
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发表时间：
2009-11-01
影响因子：
2
通讯作者：
Yashiro, Takashi
中科院分区：
文献类型：
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作者：
Fujiwara, Ken;Kikuchi, Motoshi;Yashiro, Takashi
视黄酸（RA）在胚胎发育、生长和生殖中起着关键作用。类维生素A通过氧化过程合成RA，并且由视黄醇醛脱氢酶（RALDH）催化将视黄醛氧化为RA。我们以前报道，RALDH 1 mRNA表达在成年大鼠的垂体前叶腺和抑制管理的17 β-雌二醇在体内。然而，很少有人知道垂体RALDH 1的表达调节机制。为了表征雌激素诱导的RALDH 1减少的机制，我们研究了17 β-雌二醇在体内和体外对垂体RALDH 1基因表达和蛋白质产生的调节作用。使用定量实时PCR和免疫印迹分析，我们发现，RALDH 1基因表达和蛋白质的生产水平显着下降后，1周的治疗与17 β-雌二醇在雄性大鼠。在免疫组织化学分析中，RALDH 1免疫反应在催乳素细胞和卵泡星状细胞中观察到。在17 β-雌二醇治疗的大鼠中，RALDH 1免疫反应性在催乳素细胞中较低，但在卵泡星状细胞中不低。用17 β-雌二醇（10（-14）-10（-8）M）处理离体垂体前叶细胞以剂量依赖方式降低RALDH 1 mRNA的表达。雌二醇诱导的RALDH 1表达抑制被雌激素受体（ER）拮抗剂ICT 182，780完全阻断。ER α-选择性激动剂丙基吡唑三醇（10（-8）M）模拟了17 β-雌二醇对RALDH 1表达的作用，但ER β-选择性激动剂二芳基丙腈（10（-8）M）没有。这些结果有力地表明，RALDH 1 mRNA的表达受到抑制的17 β-雌二醇通过ER α，雌激素调节RALDH 1的表达和生产的RA在垂体前叶。
Retinoic acid (RA) plays a critical role in embryonic development, growth, and reproduction. RA is synthesized from retinoids via oxidation processes, and the oxidation of retinal to RA is catalyzed by the retinaldehyde dehydrogenases (RALDHs). We previously reported that RALDH1 mRNA was expressed in the anterior pituitary glands of adult rats and suppressed by administration of 17 beta-estradiol in vivo. However, little is known about the mechanism regulating pituitary RALDH1 expression. In order to characterize the mechanism of estrogen-induced RALDH1 reduction, we examined the effect of 17 beta-estradiol on the regulation of pituitary RALDH1 gene expression and protein production both in vivo and in vitro. Using quantitative real-time PCR and immunoblot analysis, we found that levels of RALDH1 gene expression and protein production markedly decreased after 1-week treatment with 17 beta-estradiol in male rats. In immunohistochemical analysis, RALDH1-immunoreaction was observed in prolactin cells and folliculo-stellate cells. In 17 beta-estradiol-treated rats, RALDH1-immunoreactivity was lower in prolactin cells, but not in folliculo-stellate cells. Treatment of isolated anterior pituitary cells with 17 beta-estradiol (10(-14) - 10(-8) M) decreased expression of RALDH1 mRNA in a dose-dependent manner. Estradiol-induced suppression of RALDH1 expression was completely blocked by the estrogen receptor (ER) antagonist ICT 182, 780. The ER alpha-selective agonist propylpyrazole triol (10(-8) M) mimicked the effect of 17 beta-estradiol on RALDH1 expression, but the ER beta-selective agonist diarylpropionitrile (10(-8) M) did not. These results strongly suggest that RALDH1 mRNA expression is suppressed by 17 beta-estradiol through ER alpha, and that estrogen regulates the expression of RALDH1 and production of RA in the anterior pituitary gland.