在下丘脑雌二醇刺激孕激素合成星形胶质细胞的文化。
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Micevych PE、Chaban V,奥吉J,结露P, Lu JK Sinchak K
在下丘脑雌二醇刺激孕激素合成星形胶质细胞的文化。
内分泌学。2007年2月,148 (2):782 - 9。Epub 2006年11月9日。
- PubMed ID
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17095591 (在PubMed]
- 文摘
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大脑合成类固醇新创,尤其是孕激素。最近雌二醇在下丘脑刺激孕激素合成和丰富星形胶质细胞文化来源于新生儿皮层。Estradiol-induced下丘脑孕激素已经涉及LH的控制。目前的研究以确定是否进行下丘脑星形胶质细胞来源于女性新生儿或女性postpubertal老鼠增加产量的孕激素雌二醇在回应的挑战。雌二醇诱发孕激素合成postpubertal星形胶质细胞但不是新生儿星形胶质细胞。这雌二醇行动是182780年被雌激素受体拮抗剂ICI。之前我们已经表明,雌二醇刺激迅速增加在自由胞质钙(2 +)((Ca(2 +))(我))的新生儿峰值皮质星形胶质细胞通过膜雌激素受体作用。我们现在报告,雌二醇也迅速增加(Ca (2 +)) (i)峰值在下丘脑星形胶质细胞。的membrane-impermeable estradiol-BSA构造也诱导(Ca (2 +)) (i)峰值。182780年ICI estradiol-BSA和雌二醇被封锁。 Depleting intracellular Ca(2+) stores prevented the estradiol-induced increased [Ca(2+)](i) spikes, whereas removing extracellular Ca(2+) did not prevent estradiol-induced [Ca(2+)](i) spikes. Together these results indicate that estradiol acts through a membrane-associated receptor to release intracellular stores of Ca(2+). Thapsigargin, used to mimicked the intracellular release of Ca(2+) by estradiol, increased progesterone synthesis, suggesting that estradiol-induced progesterone synthesis involves increases in [Ca(2+)](i). Estradiol treatment did not change levels of steroid acute regulatory protein, P450 side chain cleavage, 3beta-hydroxysteroid dehydrogenase, and sterol carrier protein-2 mRNAs as measured by quantitative RT-PCR, suggesting that in vitro, estradiol regulation of progesterone synthesis in astrocytes does not depend on transcription of new steroidogenic proteins. The present results are consistent with our hypothesis that estrogen-positive feedback regulating the LH surge involves stimulating local progesterone synthesis by hypothalamic astrocytes.