The quantity of Sertoli cells in the adult testis decides the daily gamete formation, and accumulating evidence indicates that epigenetic factors regulate the proliferation of Sertoli cells. Research on the function and regulatory mechanism of microRNAs (miRNAs) in Sertoli cells has not been comprehensive yet, especially on domestic animals. In this article, we report that miR-126 controls the proliferation and apoptosis of immature porcine Sertoli cells based on previous studies. Our results confirmed that miR-126 elevation promotes cell cycle progression, cell proliferation and represses cell apoptosis; on the contrary, the inhibitory effects of miR-126 result in the opposite. The phosphoinositide-3-kinase regulatory subunit 2 (PIK3R2) gene, a member of the PI3K family, was verified as a direct target of miR-126 using the dual-luciferase reporter analysis. miR-126 negatively regulated the mRNA and protein expression level of PIK3R2 in immature porcine Sertoli cells. siRNA-induced PIK3R2 inhibition caused similar effects as miR-126 overexpression and eliminated the influences of miR-126 knockdown in immature porcine Sertoli cells. In addition, both miR-126 overexpression and PIK3R2 inhibition elevated the phosphorylation of PI3K and AKT, whereas the miR-126 knockdown demonstrated the contrary result. In short, miR-126 controls the proliferation and apoptosis of immature porcine Sertoli cells by targeting the PIK3R2 gene through the PI3K/AKT signaling pathway. The research supplies a theoretical and practical foundation for exploring the functional parts of miR-126 in swine sperm by defining the destiny of immature Sertoli cells.

中文翻译：

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miR-126 通过 PI3K/AKT 信号通路靶向 PIK3R2 基因控制未成熟猪支持细胞的凋亡和增殖

成年睾丸中支持细胞的数量决定了每日配子的形成，越来越多的证据表明表观遗传因素调节支持细胞的增殖。对支持细胞中 microRNA (miRNA) 的功能和调控机制的研究尚不全面，尤其是在家养动物上。在这篇文章中，我们报告了基于先前研究的 miR-126 控制未成熟猪支持细胞的增殖和凋亡。我们的结果证实，miR-126 升高促进细胞周期进程、细胞增殖并抑制细胞凋亡；相反，miR-126的抑制作用则相反。磷酸肌醇-3-激酶调节亚基 2 ( PIK3R2) 基因是 PI3K 家族的成员，使用双荧光素酶报告基因分析被证实为 miR-126 的直接靶标。miR-126在未成熟的猪支持细胞中负调控PIK3R2的 mRNA 和蛋白表达水平。siRNA 诱导的PIK3R2抑制引起与 miR-126 过表达相似的效果，并消除了未成熟猪支持细胞中 miR-126 敲低的影响。此外，miR-126 过表达和PIK3R2抑制都提高了 PI3K 和 AKT 的磷酸化，而 miR-126 敲低则显示出相反的结果。总之，miR-126通过靶向PIK3R2调控未成熟猪支持细胞的增殖和凋亡PI3K/AKT 信号通路。该研究通过定义未成熟支持细胞的命运，为探索猪精子中 miR-126 的功能部分提供了理论和实践基础。