Micro-RNA miR-542-3p suppresses decidualization by targeting ILK pathways in human endometrial stromal cells

Abstract Decidualization of human endometrial stromal cells (HESCs) is a vital step for successful pregnancy. However, the process by which micro-RNAs (miRNAs) regulate decidualization remains elusive. Our current study was designed to identify the mechanism of miRNA miR-542-3p and its potential tar...

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Autores principales: Xinlan Qu, Yuan Fang, Siying Zhuang, Yuanzhen Zhang
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Publicado: Nature Portfolio 2021
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spelling oai:doaj.org-article:748a3c0470bb4f37a8bc09bb4a8236372021-12-02T13:26:58ZMicro-RNA miR-542-3p suppresses decidualization by targeting ILK pathways in human endometrial stromal cells10.1038/s41598-021-85295-22045-2322https://doaj.org/article/748a3c0470bb4f37a8bc09bb4a8236372021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-85295-2https://doaj.org/toc/2045-2322Abstract Decidualization of human endometrial stromal cells (HESCs) is a vital step for successful pregnancy. However, the process by which micro-RNAs (miRNAs) regulate decidualization remains elusive. Our current study was designed to identify the mechanism of miRNA miR-542-3p and its potential targets in regulating decidualization. The results showed that miR-542-3p was down-regulated in HESCs. Luciferase assay confirmed that integrin-linked kinase (ILK) is a direct target of miR-542-3p. Overexpression of miR-542-3p resulted in decreased ILK and downstream transforming growth factor β1 (TGF-β1) and SMAD family member 2 (SMAD2) expression. Additional expression of ILK attenuates the miR542-3p-induced down-regulation of TGF-β1 and SMAD2, changes properties such as suppression of proliferation and invasion, and induction of apoptosis, thereby affecting the differentiation of HESCs. Moreover, miR-542-3p overexpression caused down-regulation of the angiogenic factors vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2) and matrix metalloproteinase-9 (MMP-9), and the supernatant of HESCs overexpressing miR-542-3p inhibited the formation of tubular structures in human umbilical vein endothelial cells (HUVECs), suggesting that miR-542-3p inhibits angiogenesis of HUVECs. Furthermore, in our mouse model, following injection of miR-542-3p mimic into the endometrium of mice at pregnancy day 8 (D8), we found decreased miR-542-3p expression and loss of embryo implantation sites. In conclusion, miR-542-3p can affect the process of endometrial decidualization by down-regulating ILK. The present study adds further understanding of the process and regulation of decidualization.Xinlan QuYuan FangSiying ZhuangYuanzhen ZhangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-11 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Xinlan Qu
Yuan Fang
Siying Zhuang
Yuanzhen Zhang
Micro-RNA miR-542-3p suppresses decidualization by targeting ILK pathways in human endometrial stromal cells
description Abstract Decidualization of human endometrial stromal cells (HESCs) is a vital step for successful pregnancy. However, the process by which micro-RNAs (miRNAs) regulate decidualization remains elusive. Our current study was designed to identify the mechanism of miRNA miR-542-3p and its potential targets in regulating decidualization. The results showed that miR-542-3p was down-regulated in HESCs. Luciferase assay confirmed that integrin-linked kinase (ILK) is a direct target of miR-542-3p. Overexpression of miR-542-3p resulted in decreased ILK and downstream transforming growth factor β1 (TGF-β1) and SMAD family member 2 (SMAD2) expression. Additional expression of ILK attenuates the miR542-3p-induced down-regulation of TGF-β1 and SMAD2, changes properties such as suppression of proliferation and invasion, and induction of apoptosis, thereby affecting the differentiation of HESCs. Moreover, miR-542-3p overexpression caused down-regulation of the angiogenic factors vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2) and matrix metalloproteinase-9 (MMP-9), and the supernatant of HESCs overexpressing miR-542-3p inhibited the formation of tubular structures in human umbilical vein endothelial cells (HUVECs), suggesting that miR-542-3p inhibits angiogenesis of HUVECs. Furthermore, in our mouse model, following injection of miR-542-3p mimic into the endometrium of mice at pregnancy day 8 (D8), we found decreased miR-542-3p expression and loss of embryo implantation sites. In conclusion, miR-542-3p can affect the process of endometrial decidualization by down-regulating ILK. The present study adds further understanding of the process and regulation of decidualization.
format article
author Xinlan Qu
Yuan Fang
Siying Zhuang
Yuanzhen Zhang
author_facet Xinlan Qu
Yuan Fang
Siying Zhuang
Yuanzhen Zhang
author_sort Xinlan Qu
title Micro-RNA miR-542-3p suppresses decidualization by targeting ILK pathways in human endometrial stromal cells
title_short Micro-RNA miR-542-3p suppresses decidualization by targeting ILK pathways in human endometrial stromal cells
title_full Micro-RNA miR-542-3p suppresses decidualization by targeting ILK pathways in human endometrial stromal cells
title_fullStr Micro-RNA miR-542-3p suppresses decidualization by targeting ILK pathways in human endometrial stromal cells
title_full_unstemmed Micro-RNA miR-542-3p suppresses decidualization by targeting ILK pathways in human endometrial stromal cells
title_sort micro-rna mir-542-3p suppresses decidualization by targeting ilk pathways in human endometrial stromal cells
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/748a3c0470bb4f37a8bc09bb4a823637
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AT yuanfang micrornamir5423psuppressesdecidualizationbytargetingilkpathwaysinhumanendometrialstromalcells
AT siyingzhuang micrornamir5423psuppressesdecidualizationbytargetingilkpathwaysinhumanendometrialstromalcells
AT yuanzhenzhang micrornamir5423psuppressesdecidualizationbytargetingilkpathwaysinhumanendometrialstromalcells
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