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Downregulating lncRNA NEAT1 induces proliferation and represses apoptosis of ovarian granulosa cells in polycystic ovary syndrome via microRNA-381/IGF1 axis
Journal of Biomedical Science ( IF 9.0 ) Pub Date : 2021-07-15 , DOI: 10.1186/s12929-021-00749-z
Jingran Zhen 1 , Jiangli Li 2 , Xia Li 3 , Xue Wang 1 , Yaling Xiao 1 , Zhengyi Sun 1 , Qi Yu 1
Affiliation  

Researchers have revealed the combined functions of long noncoding RNAs (lncRNAs) and microRNA (miRNAs) in polycystic ovary syndrome (PCOS). This study aimed to understand the role of nuclear-enriched abundant transcript 1 (NEAT1) and miR-381 involving insulin-like growth factor 1 (IGF1) in PCOS. PCOS rat model was established by dehydroepiandrosterone induction. NEAT1, miR-381 and IGF1 expression in ovarian granulosa cells of PCOS patients and ovarian tissues of PCOS rats were tested. Bioinformatics website and dual luciferase reporter gene assay were utilized to verify the relationship between NEAT1 and miR-381 and that between miR-381 and IGF1. Levels of sex hormone, pathological changes and ovarian granulosa cell apoptosis in ovarian tissues of PCOS rats were detected. Ovarian granulosa cell proliferation and apoptosis were analyzed in vitro. NEAT1 and IGF1 expression increased while miR-381 expression decreased in the ovarian granulosa cells of patients with PCOS and the ovarian tissues of PCOS rats. In in vivo experiments, interference with NEAT1 improved the levels of sex hormones, alleviated pathological changes and suppressed ovarian granulosa cell apoptosis in the ovarian tissues of PCOS rats. In in vitro cell experiments, interference with NEAT1 suppressed apoptosis and enhanced cell proliferation of ovarian granulosa cells. NEAT1 interference-mediated effect would be reversed by up-regulating miR-381. NEAT1 acted as a ceRNA to adsorb miR-381 to target IGF1. Overexpression of IGF1 reversed the inhibitory effect of miR-381 on ovarian granulosa cell apoptosis. Interference with NEAT1 increases miR-381 and reduces IGF1 levels, effectively improving the levels of sex hormones and reducing the pathological damage of ovarian tissue in rats with PCOS.

中文翻译:

下调lncRNA NEAT1通过microRNA-381/IGF1轴诱导多囊卵巢综合征卵巢颗粒细胞增殖并抑制凋亡

研究人员揭示了长链非编码 RNA (lncRNA) 和 microRNA (miRNA) 在多囊卵巢综合征 (PCOS) 中的综合功能。本研究旨在了解富含核的丰富转录物 1 (NEAT1) 和 miR-381 与胰岛素样生长因子 1 (IGF1) 在 PCOS 中的作用。通过脱氢表雄酮诱导建立PCOS大鼠模型。检测PCOS患者卵巢颗粒细胞和PCOS大鼠卵巢组织中NEAT1、miR-381和IGF1的表达。利用生物信息学网站和双荧光素酶报告基因检测验证 NEAT1 与 miR-381 以及 miR-381 与 IGF1 之间的关系。检测PCOS大鼠卵巢组织中性激素水平、病理变化及卵巢颗粒细胞凋亡。体外分析卵巢颗粒细胞增殖和凋亡。PCOS患者卵巢颗粒细胞和PCOS大鼠卵巢组织中NEAT1和IGF1表达增加,而miR-381表达降低。在体内实验中,干扰 NEAT1 可提高 PCOS 大鼠卵巢组织中性激素水平、减轻病理变化并抑制卵巢颗粒细胞凋亡。在体外细胞实验中,对 NEAT1 的干扰抑制了卵巢颗粒细胞的凋亡并增强了细胞增殖。NEAT1 干扰介导的作用将通过上调 miR-381 来逆转。NEAT1 作为 ceRNA 吸附 miR-381 以靶向 IGF1。IGF1的过表达逆转了miR-381对卵巢颗粒细胞凋亡的抑制作用。干扰 NEAT1 会增加 miR-381 并降低 IGF1 水平,
更新日期:2021-07-15
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