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首页> 外文期刊>Molecular reproduction and development >MCL1 is a key regulator of steroidogenesis in mouse Leydig cells
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MCL1 is a key regulator of steroidogenesis in mouse Leydig cells

机译:MCL1是小鼠Leydig细胞中类固醇生成的关键调节剂

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摘要

Myeloid cell leukemia-1 (MCL1), an anti-apoptotic member of the BCL2 family, is expressed abundantly in the testis. Previous characterization revealed that MCL1 is expressed exclusively in the Leydig cells in the mouse testis, yet what it does in these cells remains unknown. We therefore analyzed testosterone biosynthesis in isolated primary Leydig cells and the MA-10 cell line, in which MCL1 was knocked down using an siRNA strategy. The mRNA abundance of the steroidogenic genes Star, Cyp11a1, Cyp17a1, Hsd3b1, Srd5a, and the luteinizing hormone/choriogonadotropin receptor Lhcgr were significantly reduced following MCL1 knockdown. Of the two enzymes required for testosterone biosynthesis, STAR and P450 SCC (encoded by Cyp11a1) enzyme abundance was also reduced following Mcl1 siRNA treatment, possibly leading to the reduced production of sex steroid precursors, and testosterone in these knockdown cells. Despite its classification as an anti-apoptosis protein, Mcl1 siRNA treatment did not affect cell survival. Collectively, our findings indicate that MCL1 plays a pivotal role in Leydig-cell steroidogenesis, and might provide novel insights into metabolic regulation in this cell. Mol. Reprod. Dev. 83: 226-235, 2016. (c) 2016 Wiley Periodicals, Inc.
机译:骨髓细胞白血病1(MCL1),BCL2家族的抗凋亡成员,在睾丸中大量表达。先前的特征显示,MCL1仅在小鼠睾丸的Leydig细胞中表达,但在这些细胞中的作用仍然未知。因此,我们分析了分离的初级Leydig细胞和MA-10细胞系中的睾丸激素生物合成,其中使用siRNA策略敲低了MCL1。 MCL1敲低后,类固醇生成基因Star,Cyp11a1,Cyp17a1,Hsd3b1,Srd5a和促黄体生成素/促性腺激素受体Lhcgr的mRNA丰度显着降低。在Mcl1 siRNA处理后,睾丸激素生物合成所需的两种酶中,STAR和P450 SCC(由Cyp11a1编码)的酶丰度也降低了,这可能导致性类固醇前体和这些击倒细胞中睾丸激素的产生减少。尽管将其分类为抗凋亡蛋白,但Mcl1 siRNA处理并未影响细胞存活。总的来说,我们的发现表明MCL1在Leydig细胞类固醇生成中起着关键作用,并且可能为该细胞的代谢调控提供新的见解。大声笑责备。开发人员83:226-235,2016年。(c)2016 Wiley Periodicals,Inc.

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