MiR-145 regulates steroidogenesis in mouse primary granulosa cells by targeting Arpc5 and subsequent cytoskeleton remodeling.

IF 1.9 4区 生物学 Q2 AGRICULTURE, DAIRY & ANIMAL SCIENCE
Lanfang Ma, Shuo Wang, Jun Yang, Weicheng Tang, Zhangying Wu, Lili Cao, Aiyue Luo, Fangfang Fu, Shuhong Yang, Shixuan Wang
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Abstract

MicroRNA (miR)-145 is enriched in the follicular granulosa cells (GCs) of 3-week-old mice. Downregulating miR-145 inhibits the proliferation and differentiation of GCs and induces evident changes in their cytoskeleton. In this study, we examined how miR-145 induces cytoskeletal changes in mouse GCs and its potential mechanism in regulating GC steroidogenesis. We found that actin related protein 2/3 complex subunit 5 (Arpc5) is a target of miR-145. The miR-145 antagomir increased ARPC5 expression but not β-ACTIN, β-TUBULIN, and PAXILLIN expression. Arpc5 overexpression inhibited GC proliferation, differentiation, and progesterone synthesis. Furthermore, the expression of progesterone synthesis-associated enzymes was downregulated in the Arpc5 overexpression group, and the GC cytoskeleton exhibited evident changes. We conclude that Arpc5, a new target of miR-145, regulates primary GC proliferation and progesterone production by regulating the cytoskeleton remodeling.

Abstract Image

Abstract Image

Abstract Image

MiR-145通过靶向Arpc5和随后的细胞骨架重塑来调节小鼠原代颗粒细胞中的甾体生成。
MicroRNA (miR)-145在3周龄小鼠滤泡颗粒细胞(GCs)中富集。下调miR-145抑制GCs的增殖和分化,诱导其细胞骨架发生明显变化。在这项研究中,我们研究了miR-145如何诱导小鼠GC细胞骨架变化及其调节GC类固醇生成的潜在机制。我们发现肌动蛋白相关蛋白2/3复合物亚基5 (Arpc5)是miR-145的靶标。miR-145拮抗剂增加了ARPC5的表达,但没有增加β-ACTIN、β-TUBULIN和PAXILLIN的表达。Arpc5过表达抑制GC增殖、分化和黄体酮合成。Arpc5过表达组黄体酮合成相关酶表达下调,GC细胞骨架发生明显变化。我们得出结论,miR-145的新靶点Arpc5通过调节细胞骨架重塑来调节原代GC增殖和孕酮的产生。
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来源期刊
Journal of Reproduction and Development
Journal of Reproduction and Development 生物-奶制品与动物科学
CiteScore
3.70
自引率
11.10%
发文量
52
审稿时长
2 months
期刊介绍: Journal of Reproduction and Development (JRD) is the official journal of the Society for Reproduction and Development, published bimonthly, and welcomes original articles. JRD provides free full-text access of all the published articles on the web. The functions of the journal are managed by Editorial Board Members, such as the Editor-in-Chief, Co-Editor-inChief, Managing Editors and Editors. All manuscripts are peer-reviewed critically by two or more reviewers. Acceptance is based on scientific content and presentation of the materials. The Editors select reviewers and correspond with authors. Final decisions about acceptance or rejection of manuscripts are made by the Editor-in-Chief and Co-Editor-in-Chief.
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