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Identification of Genes and Pathways in the Synovia of Women with Osteoarthritis by Bioinformatics Analysis

Overview
Journal Mol Med Rep
Specialty Molecular Biology
Date 2018 Jan 19
PMID 29344651
Citations 16
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Abstract

Osteoarthritis (OA) has a high prevalence in female patients and sex may be a key factor affecting the progression of OA. The aim of the present study was to identify genetic signatures in the synovial membranes of female patients with OA and to elucidate the potential associated molecular mechanisms. The gene expression profiles of the GSE55457 and GSE55584 datasets were obtained from the Gene Expression Omnibus database. Data of two synovial membranes from normal female individuals (GSM1337306 and GSM1337310) and two synovial membranes from female patients affected by OA (GSM1337327 and GSM1337330) were obtained from the dataset GSE55457, and those of three synovial membranes from female patients affected by OA (GSM1339628, GSM1339629 and GSM1339632) were obtained from the dataset GSE55584. Differentially expressed genes (DEGs) were identified by using Morpheus software. Protein‑protein interaction (PPI) networks of the DEGs were constructed by using Cytoscape software. Subsequently, Gene Ontology (GO) function and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway enrichment analyses of the top module of the PPI network were performed by using ClueGo. A total of 377 DEGs were identified in the synovial membranes of OA patients compared with those of normal individuals, including 164 upregulated and 213 downregulated genes. The top 10 hub genes were ubiquitin (UB)C, ribosomal protein (RP) L23A, mammalian target of rapamycin, heat shock protein 90 α family class A member 1, RPS28, RPL37A, RPS24, RPS4X, RPS18 and UBB. The results of the GO analysis indicated that the DEGs included in the top module of the PPI were mainly enriched in the terms 'nuclear‑transcribed mRNA catabolic process', 'nonsense mediated decay', and 'cytoplasmic translation and ribosomal small subunit biogenesis'. KEGG pathway analysis indicated that the DEGs included in the top one module were mainly enriched in the 'ribosome' pathway. The present study provides a systematic, molecular‑level understanding of the degeneration of the synovial membrane in the progression of OA in female patients. The hub genes and molecules associated with the synovial membrane may be used as biomarkers and therapeutic targets for the treatment of OA in female patients with OA.

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