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Regulation of estrogen sulfotransferase expression by estrogen receptor alpha in mouse testis
- 언어ENG
- URLhttps://db.koreascholar.com/Article/Detail/355155
Estrogen sulfotransferase (EST) is a cytosolic enzyme that catalyzes the sulfo-conjugation of estrogens at the 3-hydroxyl position. Sulfated estrogens lose their ability to interact with the estrogen receptor (ER). Previous studies have reported that testicular expression of EST is under the regulation of LH and androgen. In an effort to understand the biological significance of estrogens in the testis, we analyzed the EST gene expression in the developing mouse testis and Leydig cells and its regulation by estrogen receptor alpha (ERα). Male mice at postnatal day (PND) 1, 7, 14, 28, and 56 and ERα flox/flox Cyp17iCre male mice which show deletion of ERα specifically in Leydig cells were used for this study. Testes and Leydig cells isolated from these mice were subjected to quantitative RT-PCR analysis and immunohistochemistry. In addition, 17β-estradiol (E2), ERα-selective agonist PPT, ERβ -selective agonist DPN, and ER antagonist ICI 182,780 were treated in primary adult Leydig cell culture. These cultured cells were subjected to quantitative RT-PCR analysis. In testis, EST mRNA level was excessively low by PND 14 and markedly increased from puberty (PND 28) onward. In the interstitium, EST mRNA was not detected by PND 14 but considerably expressed from PND 28 onward. EST immunoreactivity was moderate in the interstitium by PND 14. Strong EST immunoreactivity was found in the interstitium from PND 28 onward. In ERαflox/flox Cyp17iCre mouse testis and Leydig cells, EST mRNA level was significantly lower than wild type (ERαflox/flox). In primary adult Leydig cell culture, the expression of EST mRNA was increased by E2 and PPT, but was not changed by DPN. The expression of EST in the testis is developmentally regulated. In adult Leydig cells, EST could play an important role in the steroidogenesis by modulating the activity of estrogens. Estrogen as well as LH and androgen may play a role in the regulation of EST expression in Leydig cells via ERα signaling.
