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Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium

Although the thin endometrium (TE) has been widely recognized as a critical factor in implantation failure, the contribution of miRNA–mRNA regulatory network to the development of disease etiology remains to be further elucidated. This study performed an integrative analysis of the miRNA–mRNA expres...

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Autores principales: Zong, Lu, Zheng, Shengxia, Meng, Ye, Tang, Wenjuan, Li, Daojing, Wang, Zhenyun, Tong, Xianhong, Xu, Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8009322/
https://www.ncbi.nlm.nih.gov/pubmed/33796129
http://dx.doi.org/10.3389/fgene.2021.589408
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author Zong, Lu
Zheng, Shengxia
Meng, Ye
Tang, Wenjuan
Li, Daojing
Wang, Zhenyun
Tong, Xianhong
Xu, Bo
author_facet Zong, Lu
Zheng, Shengxia
Meng, Ye
Tang, Wenjuan
Li, Daojing
Wang, Zhenyun
Tong, Xianhong
Xu, Bo
author_sort Zong, Lu
collection PubMed
description Although the thin endometrium (TE) has been widely recognized as a critical factor in implantation failure, the contribution of miRNA–mRNA regulatory network to the development of disease etiology remains to be further elucidated. This study performed an integrative analysis of the miRNA–mRNA expression profiles in the thin and adjacent normal endometrium of eight patients with intrauterine adhesion to construct the transcriptomic regulatory networks. A total of 1,093 differentially expressed genes (DEGs) and 72 differentially expressed miRNAs (DEMs) were identified in the thin adhesive endometrium of the TE group compared with the control adjacent normal endometrial cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed that the DEGs and the target genes of DEM were significantly enriched in angiogenesis, cell growth regulation, and Wnt signaling pathway. Multiple hub genes (CAV1, MET, MAL2, has-mir-138, ARHGAP6, CLIC4, RRAS, AGFG1, has-mir-200, and has-mir-429) were identified by constructing the miRNA–mRNA regulatory networks. Furthermore, a miRNA–mRNA pathway function analysis was conducted, and the hub genes were enriched in the FoxO signaling pathway, cell growth regulation, inflammatory response regulation, and regulation of autophagy pathways. Our study is the first to perform integrated mRNA-seq and miRNA-seq analyses in the thin adhesive endometrium and the control adjacent normal endometrial cells. This study provides new insights into the molecular mechanisms underlying the formation of thin endometrium.
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spelling pubmed-80093222021-03-31 Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium Zong, Lu Zheng, Shengxia Meng, Ye Tang, Wenjuan Li, Daojing Wang, Zhenyun Tong, Xianhong Xu, Bo Front Genet Genetics Although the thin endometrium (TE) has been widely recognized as a critical factor in implantation failure, the contribution of miRNA–mRNA regulatory network to the development of disease etiology remains to be further elucidated. This study performed an integrative analysis of the miRNA–mRNA expression profiles in the thin and adjacent normal endometrium of eight patients with intrauterine adhesion to construct the transcriptomic regulatory networks. A total of 1,093 differentially expressed genes (DEGs) and 72 differentially expressed miRNAs (DEMs) were identified in the thin adhesive endometrium of the TE group compared with the control adjacent normal endometrial cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed that the DEGs and the target genes of DEM were significantly enriched in angiogenesis, cell growth regulation, and Wnt signaling pathway. Multiple hub genes (CAV1, MET, MAL2, has-mir-138, ARHGAP6, CLIC4, RRAS, AGFG1, has-mir-200, and has-mir-429) were identified by constructing the miRNA–mRNA regulatory networks. Furthermore, a miRNA–mRNA pathway function analysis was conducted, and the hub genes were enriched in the FoxO signaling pathway, cell growth regulation, inflammatory response regulation, and regulation of autophagy pathways. Our study is the first to perform integrated mRNA-seq and miRNA-seq analyses in the thin adhesive endometrium and the control adjacent normal endometrial cells. This study provides new insights into the molecular mechanisms underlying the formation of thin endometrium. Frontiers Media S.A. 2021-03-16 /pmc/articles/PMC8009322/ /pubmed/33796129 http://dx.doi.org/10.3389/fgene.2021.589408 Text en Copyright © 2021 Zong, Zheng, Meng, Tang, Li, Wang, Tong and Xu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Genetics
Zong, Lu
Zheng, Shengxia
Meng, Ye
Tang, Wenjuan
Li, Daojing
Wang, Zhenyun
Tong, Xianhong
Xu, Bo
Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium
title Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium
title_full Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium
title_fullStr Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium
title_full_unstemmed Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium
title_short Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium
title_sort integrated transcriptomic analysis of the mirna–mrna interaction network in thin endometrium
topic Genetics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8009322/
https://www.ncbi.nlm.nih.gov/pubmed/33796129
http://dx.doi.org/10.3389/fgene.2021.589408
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