Abstract

Polycystic ovary syndrome (PCOS) is a common endocrinopathy related to female infertility. We investigated the function of the microRNA-98-3p (miR-98-3p)/Yin-Yang-1 (YY1) axis to the pathophysiological processes in PCOS mice. A mouse model of PCOS was established using dehydroepiandrosterone (DHEA). Hematoxylin and eosin (HE) staining was used to assess morphologic changes of the ovaries. Hormonal serum levels were measured by ELISA. Estrogen synthesis in OGCs was measured using chemiluminescence immunoassay. The viability, cell cycle, and apoptosis of ovarian granulosa cells (OGCs) were assessed by CCK-8, flow cytometry, and western blot. Luciferase reporter assays were conducted to examine the binding of miR-98-3p to YY1. YY1 was upregulated, while miR-98-3p was downregulated both in the ovarian tissues of PCOS mice and OGCs separated from PCOS mice and patients. YY1 Knockdown promoted OGC proliferation and inhibited apoptosis as well as increased estrogen production in OGCs. YY1 was verified to be targeted by miR-98-3p. Additionally, YY1 overexpression prevented the effects of miR-98-3p overexpression on the proliferation and apoptosis of OGCs. Importantly, miR-98-3p attenuated ovarian injury in PCOS mice. MiR-98-3p targets and downregulates YY1 expression, thereby affecting the proliferation and apoptosis of OGCs in PCOS.

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