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首页> 外文期刊>Endocrinology >Involvement of the thromboxane A2 receptor in the regulation of steroidogenic acute regulatory gene expression in murine Leydig cells.
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Involvement of the thromboxane A2 receptor in the regulation of steroidogenic acute regulatory gene expression in murine Leydig cells.

机译：血栓烷A2受体参与小鼠Leydig细胞中类固醇生成的急性调节基因表达的调节。

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摘要

Recent studies suggested an involvement of thromboxane A2 in cyclooxygenase-2-dependent inhibition of steroidogenic acute regulatory (StAR) gene expression. The present study further investigated the role of thromboxane A2 receptor in StAR gene expression and steroidogenesis in testicular Leydig cells. The thromboxane A2 receptor was detected in several Leydig cell lines. Blocking thromboxane A2 binding to the receptor using specific antagonist SQ29548 or BM567 resulted in dose-dependent increases in StAR protein and steroid production in MA-10 mouse Leydig cells. The results were confirmed with Leydig cells isolated from rats. StAR promoter activity and StAR mRNA level in the cells were also increased after the treatments, suggesting an involvement of the thromboxane A2 receptor in StAR gene transcription. Furthermore study indicated that blocking the thromboxane A2 receptor reduced dosage sensitive sex reversal-adrenal hypoplasia congenita critical region on the X chromosome, gene 1 protein, a transcriptional repressor of StAR gene expression. Specific binding of the antagonists to the receptors on cellular membrane was demonstrated by binding assays using (3)H-SQ29548 and binding competition between (3)H-SQ29548 and BM567. Whereas SQ29548 enhanced cAMP-induced StAR gene expression, in the absence of cAMP, it was unable to increase StAR protein and steroidogenesis. However, when the receptor was blocked by the antagonist, subthreshold levels of cAMP were able to induce maximal levels of StAR protein expression, suggesting that blocking the thromboxane A2 receptor increase sensitivity of MA-10 cells to cAMP stimulation. Taken together, the results from the present and previous studies suggest an autocrine loop, involving cyclooxygenase-2, thromboxane A synthase, and thromboxane A2 and its receptor, in cyclooxygenase-2-dependent inhibition of StAR gene expression.
机译：最近的研究表明血栓烷A2参与环氧化酶2依赖性抑制类固醇生成的急性调节（StAR）基因表达。本研究进一步研究了血栓烷A2受体在睾丸Leydig细胞中StAR基因表达和类固醇生成中的作用。在几种Leydig细胞系中检测到了血栓烷A2受体。使用特异性拮抗剂SQ29548或BM567阻断血栓烷A2与受体的结合会导致MA-10小鼠Leydig细胞中StAR蛋白和类固醇生成的剂量依赖性增加。从大鼠分离的Leydig细胞证实了该结果。处理后，细胞中的StAR启动子活性和StAR mRNA水平也增加，表明血栓烷A2受体参与StAR基因转录。进一步的研究表明，阻断血栓烷A2受体可降低剂量敏感性X染色体上的性逆转-肾上腺皮质发育不全先天性关键区域，即基因1蛋白，StAR基因表达的转录阻遏物。通过使用（3）H-SQ29548的结合测定以及（3）H-SQ29548和BM567之间的结合竞争证明了拮抗剂与细胞膜上受体的特异性结合。尽管SQ29548增强了cAMP诱导的StAR基因表达，但在不存在cAMP的情况下，它无法增加StAR蛋白和类固醇生成。然而，当受体被拮抗剂阻断时，亚阈水平的cAMP能够诱导StAR蛋白表达的最大水平，这表明阻断血栓烷A2受体会增加MA-10细胞对cAMP刺激的敏感性。两者合计，从当前和以前的研究结果表明涉及环加氧酶2依赖StAR基因表达的自分泌环，涉及环氧合酶2，血栓烷A合酶和血栓烷A2及其受体。

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