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miR-203 通过抑制 VEGFA 的表达促进子痫前期的发生。

miR‑203 contributes to pre‑eclampsia via inhibition of VEGFA expression.

机构信息

The First Department of Gynecology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Department of Gynecology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China.

出版信息

Mol Med Rep. 2018 Apr;17(4):5627-5634. doi: 10.3892/mmr.2018.8558. Epub 2018 Feb 2.

DOI:10.3892/mmr.2018.8558
PMID:29436641
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5866003/
Abstract

Pre-eclampsia (PE) is a common but complex condition that can occur in pregnancy. It is estimated to affect 3-8% of pregnancies worldwide. PE development is thought to be multifactorial and to involve the dysregulation of microRNA (miR) expression. However, the precise mechanisms of PE development remain unclear. The present study aimed to illustrate the association between miR‑203 expression and PE development in samples of human placenta collected from mothers with (n=18) and without (n=20) PE. It was demonstrated that miR‑203 expression was significantly increased in the PE placenta compared with the normal placenta samples, while the expression of vascular endothelial growth factor A (VEGFA) was decreased. In vitro experiments revealed that miR‑203 overexpression significantly downregulated VEGFA expression and inhibited the proliferation, migration and invasion ability of HTR‑8/SVneo cells. Suppression of miR‑203 expression alleviated these effects. A luciferase reporter assay confirmed the interaction of the 3'‑untranslated region of VEGFA with miR‑203. Thus, miR‑203 may have significant contribution to the development of PE by targeting VEGFA in the human placenta and may have potential as a biomarker or therapeutic target in the treatment of PE.

摘要

子痫前期(PE)是一种常见但复杂的妊娠疾病,估计全球有 3-8%的妊娠受到影响。PE 的发展被认为是多因素的,并涉及 microRNA(miR)表达的失调。然而,PE 发展的确切机制仍不清楚。本研究旨在说明从患有(n=18)和不患有(n=20)PE 的母亲采集的人胎盘样本中 miR-203 表达与 PE 发展之间的关联。结果表明,与正常胎盘样本相比,PE 胎盘 miR-203 表达显著增加,而血管内皮生长因子 A(VEGFA)的表达减少。体外实验表明,miR-203 过表达显著下调 VEGFA 表达并抑制 HTR-8/SVneo 细胞的增殖、迁移和侵袭能力。抑制 miR-203 表达减轻了这些作用。荧光素酶报告基因检测证实 VEGFA 的 3'非翻译区与 miR-203 相互作用。因此,miR-203 可能通过靶向人胎盘中的 VEGFA 对 PE 的发展有重要贡献,并可能作为治疗 PE 的生物标志物或治疗靶点具有潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/337a/5866003/9c7faaa04091/MMR-17-04-5627-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/337a/5866003/5856106429f5/MMR-17-04-5627-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/337a/5866003/7a95b8b8dd7e/MMR-17-04-5627-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/337a/5866003/c3381222a8cf/MMR-17-04-5627-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/337a/5866003/48db0d4afcf0/MMR-17-04-5627-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/337a/5866003/9c7faaa04091/MMR-17-04-5627-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/337a/5866003/5856106429f5/MMR-17-04-5627-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/337a/5866003/7a95b8b8dd7e/MMR-17-04-5627-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/337a/5866003/c3381222a8cf/MMR-17-04-5627-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/337a/5866003/48db0d4afcf0/MMR-17-04-5627-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/337a/5866003/9c7faaa04091/MMR-17-04-5627-g04.jpg

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