Integrated Transcriptomic Analysis of the miRNA-mRNA Interaction Network in Thin Endometrium [RNA-Seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA673823 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12964633_1.fastq.gz | Fastqsanger.gz | |||
| SRR12964633_2.fastq.gz | Fastqsanger.gz | |||
| SRR12964634_1.fastq.gz | Fastqsanger.gz | |||
| SRR12964634_2.fastq.gz | Fastqsanger.gz |
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Project 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 aetiology 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 8 patients with intrauterine adhesion to construct the transcriptomic regulatory networks. A total of 1093 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 DEGs and the target genes of DEM were significantly enriched in angiogenesis, cell growth regulation and Wnt signalling 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 signalling 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.
2021-04-07 | GSE160634 | GEO
Project 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 aetiology 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 8 patients with intrauterine adhesion to construct the transcriptomic regulatory networks. A total of 1093 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 DEGs and the target genes of DEM were significantly enriched in angiogenesis, cell growth regulation and Wnt signalling 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 signalling 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.
2021-04-07 | GSE160633 | GEO
Project description:Integrated Transcriptomic Analysis of the miRNA-mRNA Interaction Network in Thin Endometrium
| PRJNA673818 | ENA
Project description:Integrated Transcriptomic Analysis of the miRNA-mRNA Interaction Network in Thin Endometrium [miRNA-seq]
| PRJNA673824 | ENA
Project 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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Project description:This SuperSeries is composed of the SubSeries listed below.
2021-04-07 | GSE160635 | GEO
Project description:The pathophysiology of endometriotic lesion development remains unclear but involves a complex interaction between ectopic endometrium and host peritoneal tissues. We hypothesised that disruption of this interaction was likely to suppress endometriotic lesion formation. We hoped to delineate the molecular and cellular dialogue between ectopic human endometrium and peritoneal tissues in nude mice, as a first step towards testing this hypothesis. Human endometrium was xenografted into nude mice and the resulting lesions were analysed using microarrays. A novel technique was developed that unambiguously determined whether RNA transcripts identified by the microarray analyses originated from human cells (endometrium) or mouse cells (stroma). Four key pathways (ubiquitin/proteosome, inflammation, tissue remodelling/repair and ras-mediated oncogenesis) were revealed, that demonstrated communication between host stromal cells and ectopic endometrium. Keywords: Disease state analysis
2008-12-22 | GSE11691 | GEO
Project description:The pathophysiology of endometriotic lesion development remains unclear but involves a complex interaction between ectopic endometrium and host peritoneal tissues. We hypothesised that disruption of this interaction was likely to suppress endometriotic lesion formation. We hoped to delineate the molecular and cellular dialogue between ectopic human endometrium and peritoneal tissues in nude mice, as a first step towards testing this hypothesis. Human endometrium was xenografted into nude mice and the resulting lesions were analysed using microarrays. A novel technique was developed that unambiguously determined whether RNA transcripts identified by the microarray analyses originated from human cells (endometrium) or mouse cells (stroma). Four key pathways (ubiquitin/proteosome, inflammation, tissue remodelling/repair and ras-mediated oncogenesis) were revealed, that demonstrated communication between host stromal cells and ectopic endometrium. Experiment Overall Design: Paired samples of eutopic and ectopic endometrium from 9 individual women were collected and the transcript profiles compared.
2009-01-02 | E-GEOD-11691 | biostudies-arrayexpress