Down-regulation of CORO1C mediated by lncMALAT1/miR-133a-3p axis contributes to trophoblast dysfunction and preeclampsia

IF 3 2区 医学 Q2 DEVELOPMENTAL BIOLOGY Placenta Pub Date : 2024-09-10 DOI:10.1016/j.placenta.2024.09.007
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Abstract

Introduction

Placental trophoblast dysfunction has been proved to be closely related to the pathogenesis of preeclampsia. Coronaryxin-like actin-binding protein 1C (CORO1C) plays an important role in cell proliferation, apoptosis, invasion, and signal transduction, but its involvement in trophoblast dysfunction and preeclampsia remains uncertain.

Methods

The expression of CORO1C in placental tissues of preeclampsia (PE) pregnant women and pregnant mice PE model were detected by real-time quantitative polymerase chain reaction (RT-qPCR), western blotting (WB) and immunohistochemical (IHC) staining. Next, the proliferation, invasion, migration and apoptosis were performed to explore the functions of CORO1C in HTR8/SVneo cell. Furthermore, the expression of CORO1C were detected in lncMALAT1 knockdown and overexpression HTR-8/SVneo cell. And then we investigated the possible regulatory mechanism of lncMALAT1 on CORO1C through bioinformatics analysis, FISH assays, RIP assays, RNA pull down and dual luciferase reporter assays. Finally, we further validated that lncMALAT1 regulate the function of placental trophoblast cells through CORO1C.

Results

The expression of CORO1C was significantly decreased in the placenta of PE patients and mice model, and positively associated with neonatal birth weight. And we found that CORO1C inhibited trophoblast proliferation, migration and invasion. Furthermore, reduced expression of lncMALAT1 impaired CORO1C level, thereby resulting in trophoblast dysfunction. Mechanistically, the dysregulation of lncMALAT1 promoted the expression of miR-133a-3p, strongly enhancing its binding to the 3′UTR region of CORO1C mRNA for degradation.

Discussion

This study demonstrated that the dysregulation of CORO1C via lncMALAT1/miR-133a-3p axis impairs trophoblast function and contributes to preeclampsia pathogenesis, providing novel insights in PE therapy through modulating CORO1C level.

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lncMALAT1/miR-133a-3p轴介导的CORO1C下调导致滋养细胞功能障碍和子痫前期
导言:胎盘滋养层功能障碍已被证实与子痫前期的发病机制密切相关。冠突蛋白样肌动蛋白结合蛋白1C(CORO1C)在细胞增殖、凋亡、侵袭和信号转导中发挥着重要作用,但其在滋养细胞功能障碍和子痫前期中的参与仍不确定。方法 通过实时定量聚合酶链式反应(RT-qPCR)、免疫印迹(WB)和免疫组化(IHC)染色检测CORO1C在子痫前期(PE)孕妇和妊娠小鼠PE模型胎盘组织中的表达。接着,研究人员对HTR8/SVneo细胞的增殖、侵袭、迁移和凋亡进行了研究,以探讨CORO1C在HTR8/SVneo细胞中的功能。此外,我们还检测了CORO1C在lncMALAT1敲除和过表达HTR-8/SVneo细胞中的表达。然后,我们通过生物信息学分析、FISH 检测、RIP 检测、RNA pull down 和双荧光素酶报告实验研究了 lncMALAT1 对 CORO1C 的可能调控机制。结果CORO1C在PE患者和小鼠模型胎盘中的表达显著下降,并与新生儿出生体重呈正相关。我们还发现,CORO1C 可抑制滋养细胞的增殖、迁移和侵袭。此外,lncMALAT1的表达减少会降低CORO1C的水平,从而导致滋养层功能障碍。讨论 本研究表明,通过lncMALAT1/miR-133a-3p轴对CORO1C的失调会损害滋养细胞功能,并导致子痫前期发病,这为通过调节CORO1C水平来治疗子痫前期提供了新的思路。
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来源期刊
Placenta
Placenta 医学-发育生物学
CiteScore
6.30
自引率
10.50%
发文量
391
审稿时长
78 days
期刊介绍: Placenta publishes high-quality original articles and invited topical reviews on all aspects of human and animal placentation, and the interactions between the mother, the placenta and fetal development. Topics covered include evolution, development, genetics and epigenetics, stem cells, metabolism, transport, immunology, pathology, pharmacology, cell and molecular biology, and developmental programming. The Editors welcome studies on implantation and the endometrium, comparative placentation, the uterine and umbilical circulations, the relationship between fetal and placental development, clinical aspects of altered placental development or function, the placental membranes, the influence of paternal factors on placental development or function, and the assessment of biomarkers of placental disorders.
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