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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Role of hypoxia in the regulation of periovulatory EDN2 expression in the mouse.
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Role of hypoxia in the regulation of periovulatory EDN2 expression in the mouse.

机译：缺氧在小鼠围排卵期EDN2表达调控中的作用。

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We have previously proposed endothelin-2 (EDN2) as a granulosa cell-derived contractile signal that facilitates ovulation. Spatially, Edn2 mRNA expression is restricted to granulosa cells of periovulatory follicles. Temporally, mRNA for this contractile peptide is expressed immediately before follicle rupture. The primary objective of this study was to test the hypothesis that hypoxia mediates EDN2 expression in granulosa cells at ovulation, and if it does, to determine the region within the promoter responsible for this effect. To determine the effect of hypoxia on mRNA expression, immature mice were treated with 5 IU of PMSG followed 48 h later by 5 IU of human chorionic gonadotropin (hCG). Granulosa cells were isolated at 9 h after hCG, cultured under normal or hypoxic conditions, and the expression level of mRNA was compared. mRNA expression was increased when granulosa cells were cultured in a hypoxic environment (p0.05). Subsequent promoter analysis found that the 5' upstream region of the EDN2 promoter (between -1894 bp and -1407 bp) was responsible for hypoxia-mediated changes in EDN2 expression. This promoter region contains multiple sites for potential transcriptional regulation, including that by hypoxia-inducible factor 1 (HIF-1, ACGTG) at -1297 bp. The second objective of this study was to determine whether the progesterone receptor (PR) or cyclooxygenase-2 (COX-2), two key regulators of periovulatory events, controlled EDN2 expression. To accomplish this, gonadotropin-primed mice were treated with RU-486 or indomethacin and expression of mRNA for Edn2 was determined in ovaries collected at 12 h after hCG. Treatment with RU-486 or indomethacin did not affect expression of mRNA for Edn2 (p0.05). Taken together, we believe that hypoxia, but not the PR or COX-2, regulate gonadotropin-induced EDN2 expression in the periovulatory follicle.
机译：我们以前曾提出内皮素2（EDN2）作为颗粒细胞衍生的收缩信号，有助于排卵。在空间上，Edn2 mRNA表达仅限于排卵性卵泡的颗粒细胞。暂时地，在卵泡破裂之前表达该可收缩肽的mRNA。这项研究的主要目的是检验以下假设：缺氧在排卵时介导EDN2在颗粒细胞中的表达，如果确实如此，则确定启动子内负责这种作用的区域。为了确定缺氧对mRNA表达的影响，用5 IU PMSG处理未成熟小鼠，然后48小时后用5 IU人绒毛膜促性腺激素（hCG）治疗。 hCG后9小时分离颗粒细胞，在正常或低氧条件下培养，比较mRNA的表达水平。在缺氧环境中培养颗粒细胞时，mRNA表达增加（p <0.05）。随后的启动子分析发现，EDN2启动子的5'上游区域（-1894 bp和-1407 bp之间）是EDN2表达缺氧介导的变化的原因。该启动子区域包含多个潜在的转录调控位点，包括缺氧诱导因子1（HIF-1，ACGTG）的-1297 bp调控位点。这项研究的第二个目标是确定孕激素受体（PR）或环氧合酶2（COX-2）是围排卵事件的两个关键调节因子，是控制EDN2表达。为此，用RU-486或吲哚美辛处理促性腺激素引发的小鼠，并在hCG后12小时收集的卵巢中测定Edn2的mRNA表达。 RU-486或消炎痛治疗不影响Edn2的mRNA表达（p> 0.05）。两者合计，我们认为缺氧，但不是PR或COX-2，调节促性腺激素诱导的ENO2在排卵周卵泡中的表达。

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