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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其凋亡。

Downregulating lncRNA NEAT1 induces proliferation and represses apoptosis of ovarian granulosa cells in polycystic ovary syndrome via microRNA-381/IGF1 axis.

机构信息

Department of Gynecological Endocrinology and Reproduction Center, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, 41 Damucang Hutong, Xicheng, Beijing, China.

Department of Obstetrics and Gynecology, Zhongguancun Hospital, Beijing, 100080, China.

出版信息

J Biomed Sci. 2021 Jul 15;28(1):53. doi: 10.1186/s12929-021-00749-z.

DOI:10.1186/s12929-021-00749-z
PMID:34266430
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8281489/
Abstract

OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

摘要

目的：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）中的联合作用。本研究旨在探讨核富集丰富转录物 1（NEAT1）和 miR-381 涉及胰岛素样生长因子 1（IGF1）在 PCOS 中的作用。

方法：采用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 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情况，体外分析卵巢颗粒细胞增殖和凋亡。

结果：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，miR-381 表达降低。体内实验中，干扰 NEAT1 可改善 PCOS 大鼠卵巢组织中性激素水平，减轻病理变化，抑制卵巢颗粒细胞凋亡。体外细胞实验中，干扰 NEAT1 可抑制卵巢颗粒细胞凋亡，促进细胞增殖。上调 miR-381 可逆转干扰 NEAT1 介导的作用。NEAT1 作为 ceRNA 吸附 miR-381 以靶向 IGF1。过表达 IGF1 可逆转 miR-381 对卵巢颗粒细胞凋亡的抑制作用。

结论：干扰 NEAT1 可增加 miR-381 并降低 IGF1 水平，有效改善 PCOS 大鼠性激素水平，减轻卵巢组织病理损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/6d01801224cf/12929_2021_749_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/026eb04e38e5/12929_2021_749_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/be2c422067c1/12929_2021_749_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/e981c614eefe/12929_2021_749_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/3104b751c5ee/12929_2021_749_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/5dc8fccbd115/12929_2021_749_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/6424e2caf872/12929_2021_749_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/43f9af029388/12929_2021_749_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/6d01801224cf/12929_2021_749_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/026eb04e38e5/12929_2021_749_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/8c016080f437/12929_2021_749_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/be2c422067c1/12929_2021_749_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/e981c614eefe/12929_2021_749_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/3104b751c5ee/12929_2021_749_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/5dc8fccbd115/12929_2021_749_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/6424e2caf872/12929_2021_749_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/43f9af029388/12929_2021_749_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0616/8281489/6d01801224cf/12929_2021_749_Fig9_HTML.jpg

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[3]
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[4]
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[5]
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J Ovarian Res. 2023-8-23

[6]
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J Ovarian Res. 2023-7-7

[7]
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[8]
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[9]
LncRNA NEAT1 and MALAT1 are involved in polycystic ovary syndrome pathogenesis by functioning as competing endogenous RNAs to control the expression of PCOS-related target genes.

Noncoding RNA Res. 2023-3-3

[10]
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本文引用的文献

[1]
Overexpression of miR-381-3p promotes the recovery of spinal cord injury.

Eur Rev Med Pharmacol Sci. 2018-9

[2]
The role of MiR-324-3p in polycystic ovary syndrome (PCOS) via targeting WNT2B.

Eur Rev Med Pharmacol Sci. 2018-6

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Onco Targets Ther. 2016-3-7

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