The oestrogens have been highly implicated in the fertility of female animals. It is widely known that the oestrogens are primarily synthetized by the ovarian granulosa cells (GCs), and the final and essential step of this process is to catalyse the oestrone to the more active oestradiol by the protein coded by hydroxysteroid 17‐beta dehydrogenase 1 (HSD17B1) gene. However, the molecular mechanism regarding the transcription of HSD17B1 remains to be fully elucidated in ovarian GCs. In this study, the 5’‐deletion, luciferase assay and chromatin immunoprecipitation (ChIP) were utilized to explore the molecular regulation of transcription of HSD17B1 with the porcine ovarian GCs as the cellular model. After the deletions with −2105 to −1754 bp, −1753 to −1429 bp, −1430 to −1081 bp and −1082 to −730 bp, the relative luciferase activity of HSD17B1 promoter did not change significantly, but the deletion of −731 to −332 bp significantly increased the relative luciferase activity of HSD17B1 promoter, and an insertion (GTTT) that might raise the transcription of HSD17B1 was identified at −401 bp of HSD17B1. These findings suggested the region from −731 to +38 bp was the core promoter of HSD17B1, and the region between −731 to −332 bp might be a silence element for HSD17B1. Furthermore, the forkhead box A2 (FoxA2) directly bound at −412 to −401 bp to negatively but p53 bound at −383 to −374 bp to positively regulate the transcription and translation of HSD17B1 in ovarian GCs. These findings will improve our understanding on HSD17B1‐mediated oestrogens and provide useful information for further investigations into fertility of females.

中文翻译：

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FoxA2和p53调节猪卵巢颗粒细胞中HSD17B1的转录

雌激素与雌性动物的生育能力高度相关。众所周知，雌激素主要是由卵巢颗粒细胞（GCs）合成的，该过程的最后也是必不可少的步骤是通过羟基类固醇17-β脱氢酶1编码的蛋白质将雌酮催化为活性更高的雌二醇。HSD17B1）基因。然而，有关HSD17B1转录的分子机制仍有待在卵巢GC中充分阐明。在这项研究中，利用5'缺失，荧光素酶测定和染色质免疫沉淀（ChIP）来探索HSD17B1转录的分子调控。以猪卵巢GC为细胞模型。在缺失了-2105至-1754 bp，−1753至-1429 bp，−1430至−1081 bp和−1082至−730 bp后，HSD17B1启动子的相对荧光素酶活性没有明显变化，但缺失了-731至-332碱基对显著增加的相对荧光素酶活性HSD17B1启动子，和可能提高的转录插入（GTTT）HSD17B1在-401碱基对被确定HSD17B1。这些结果表明，从-731该区域38 bp的是的核心启动子HSD17B1，以及-332 bp的-731之间的区域可能是一个沉默元件HSD1 7 B1。此外，叉头盒A2（FoxA2）直接在-412至-401 bp处负结合，而p53在-383至-374 bp处正调控卵巢癌GC中HSD17B1的转录和翻译。这些发现将增进我们对HSD17B1介导的雌激素的了解，并为进一步研究雌性生育能力提供有用的信息。