Polycystic ovary syndrome (PCOS) is a hormonal disorder common among women of reproductive age. Although much is understood concerning the pathology of PCOS, further investigation into the influence of microribonucleic acids (miRNAs) on the proliferation of ovarian granulosa cells (GCs) is needed. This study investigated the role of specific miRNAs in ovarian dysfunction of PCOS and its effect on the proliferation of GCs. Initially, miRNA profiling was performed on the ovarian cortexes of 15 rats in which PCOS had been induced and 15 rats without PCOS (non-PCOS). This mechanical study was performed on ovarian GCs extracted from human chorionic gonadotrophin (hCG)-induced rats. Insulin was used to treat GCs to establish the PCOS cell model. Increased Equus caballus mir-9119 expression was observed and confirmed in the insulin-induced model of PCOS in GCs (GC-PCOS) as well as in the hCG-induced rats when compared to non-PCOS rats and cells. Observation and confirmation were carried out through both miRNA array and quantitative PCR. In contrast, downregulation of the nuclear factor kappa B (NFκB) p65 was observed in the PCOS cell model. Additionally, annexin V, FITC, and propidium iodide flow cytometry showed overexpression of miR-9119-induced apoptosis. In this study, we revealed that miR-9119 inhibition regulates p65 expression levels in insulin-treated GCs by binding to the 3'-untranslated of p65. Additionally, regulation of p65 expression was positively correlated with the expression of the double-stranded RNA endoribonuclease DICER. Moreover, RNA silencing/overexpression of p65 affected the functional role of miR-9119. In conclusion, GCs of PCOS, the expression of miR-9119, and targeted NFκB/p65-DICER axis are upregulated in order to maintain cell viability and prevent apoptosis, thereby promoting Anti-Müllerian hormone production in GCs. This study may provide a new understanding of the mechanism of GC dysfunction.

中文翻译：

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MicroRNA-9119通过介导Dicer表达来调节多囊卵巢综合征中颗粒细胞的细胞活力。

多囊卵巢综合征（PCOS）是一种育龄妇女常见的激素疾病。尽管人们对PCOS的病理学了解很多，但仍需要进一步研究微核糖核酸（miRNA）对卵巢颗粒细胞（GCs）增殖的影响。这项研究调查了特定的miRNA在PCOS卵巢功能障碍中的作用及其对GC增殖的影响。最初，对15只诱导PCOS的大鼠和15只无PCOS（非PCOS）的大鼠的卵巢皮质进行miRNA分析。这项力学研究是在从人绒毛膜促性腺激素（hCG）诱导的大鼠中提取的卵巢GC上进行的。胰岛素用于治疗GC，以建立PCOS细胞模型。与非PCOS大鼠和细胞相比，在GCs（GC-PCOS）以及hCG诱导的PCOS胰岛素诱导的PCOS模型中，观察到并证实了马球mir-9119的表达增加。通过miRNA阵列和定量PCR进行观察和确认。相反，在PCOS细胞模型中观察到核因子κB（NFκB）p65的下调。此外，膜联蛋白V，FITC和碘化丙啶流式细胞仪显示miR-9119诱导的细胞凋亡过度表达。在这项研究中，我们揭示了miR-9119抑制通过与p65的3'-非翻译结合来调节胰岛素处理的GC中p65的表达水平。此外，p65表达的调节与双链RNA核糖核酸内切酶DICER的表达呈正相关。而且，p65的RNA沉默/过表达影响miR-9119的功能。总之，为了维持细胞活力并防止细胞凋亡，PCOS的GC，miR-9119的表达以及靶向的NFκB/ p65-DICER轴被上调，从而促进GC中抗苗勒氏激素的产生。这项研究可能会提供新的认识GC功能障碍的机制。