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. 2017 Oct;16(4):4803-4810.
doi: 10.3892/mmr.2017.7188. Epub 2017 Aug 7.

Bioinformatic analysis of microRNA-mRNA expression profiles of bladder tissue induced by bladder outlet obstruction in a rat model

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Bioinformatic analysis of microRNA-mRNA expression profiles of bladder tissue induced by bladder outlet obstruction in a rat model

Liu Jian Duan et al. Mol Med Rep. 2017 Oct.

Abstract

Various microRNAs (miRNAs) have previously been demonstrated to exhibit an association with the process of bladder remodeling, induced by bladder outlet obstruction (BOO). However, little is known about miRNA and gene expression profiles and the molecular mechanism underlying bladder pathophysiological alterations. The present study used bioinformatic analysis technology to examine the altered miRNA and mRNA expression profiles of bladder tissue in a rat model of BOO and validate the involved signaling pathways. The gene expression profile data was downloaded from Gene Expression Omnibus (GEO), and the differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMs) were screened. Potential target genes of DEMs were predicted. The target genes and DEGs were used for further gene ontology (GO) analysis followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis using the Database for Annotation, Visualization and Integrated Discovery. The present study additionally constructed a DEM‑DEG interaction network. A total of 9 DEMs (3 upregulated and 6 downregulated) were identified; 664 DEGs were screened. KEGG analysis revealed that the DEGs were involved in the regulation of the actin cytoske-leton, extracellular matrix (ECM) remodeling, cell adhesion and the cell cycle. Additionally, KEGG classification indicated that these genes were important in angiogenesis, and in the p53 and transforming growth factor‑β signaling pathways. Notably, rno‑miRNA (miR)‑26b and rno‑miR‑101b were the two larger nodes of the 7 obstruction‑associated DEMs and interacted with 32 and 27 DEGs, respectively. On removal of obstruction, few DEMs were present; however, 370 genes exhibited the opposite expression trend. The majority of pathways enriched for the DEGs were identified and were associated with ECM‑receptor interaction and focal adhesion. In the DEM‑DEG regulatory network, miR‑495, miR‑494 and their target genes were significantly differentially expressed. The present study demonstrated that miRNAs and genes may be potential biomarkers of bladder remodeling induced by BOO, and additionally provided novel insights into the molecular mechanisms underlying this disorder.

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