Bioinformatics analysis of TNF-α-induced osteoarthritis cell model through microarray analysis of gene expression profiles
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(Jianghan University, Wuhan 430056, China)

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R-33

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    Abstract:

    Objective Osteoarthritis (OA) is the most common type of degenerative chronic joint disease, butthe exact genetic mechanisms are still unclear. The aim of this study was to analyze the gene expression profile in an OAcell model detected using a gene chip, and to provide a biological basis for the pathogenesis of OA. Methods Primarymouse chondrocytes were isolated using trypsin combined with collagenase, and the cells were incubated with 50 ng/ mLTNF-α for 24 h. Total RNA was extracted from the harvested cells for gene chip detection to identify differentially expressedgenes (DEGs). A fold change (FC) greater than two and P<0. 01 were the conditions required for each DEG. Biologicalinformation software was used to conduct gene ontology (GO) and KEGG pathway annotation analysis of DEGs. Results After TNF-α treatment, a total of 8096 up-regulated DEGs and 6413 down-regulated DEGs were identified, including genesthat are known to be associated with OA, such as matrix metalloproteinase, inflammatory factors, and apoptosis-related andosteoblast-related genes. In addition, Olfml1 and other olfactomedin superfamily members, Nf1 and other previouslyunreported genes related to OA, were also found. In particular, abnormal expression of a large number of genes related tocytochrome C superfamily members was found, suggesting that mitochondria-related functional genes and signaling pathwaysmay be significantly associated with OA. Conclusions The changes in the gene expression profile in a TNF-α induced OAchondrocyte model at the level of the transcriptome are datected in this study, providing new insights into the pathogenesis of OA.

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History
  • Received:December 15,2018
  • Revised:
  • Adopted:
  • Online: August 01,2019
  • Published: