Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 71, Issue -, Pages 233-240Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2019.03.037
Keywords
Osteoarthritis; ciRS-7; miR-7; Apoptosis; Inflammation
Categories
Funding
- National Natural Science Foundation of China [81702179]
- Major scientific and technological project of Changzhou municipal commission of health and family planning [ZD201809]
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Osteoarthritis (OA) is a degenerative joint disease caused by articular cartilage degradation and joint inflammation, with considerable involvement of microRNAs and circular RNAs. However, the precise role of the ciRS-7/miR-7 axis within OA still requires further elucidation. In this study, quantitative reverse-transcription PCR (qRT-PCR) was utilized to determine the relative expression of ciRS-7 and miR-7 in blood samples from OA patients compared with those from healthy individuals. Human OA chondrocytes (C28/12 cell line) were transfected with ciRS-7-siRNA, ciRS-7-cDNA, inhibitor or miR-7 mimic to investigate the influence of ciRS-7/ miR-7 expression on chondrocyte apoptosis, inflammation and related signaling pathways. Decreased ciRS-7 expression and increased miR-7 expression were observed in OA blood samples. IL-1 beta exposure of chondrocytes significantly inhibited proliferation and promoted inflammatory cytokine release. ciRS-7 was down-regulated but miR-7 was up-regulated in IL-1 beta-induced chondrocytes. Transfection of ciRS-7 siRNA and miR-7 mimic enhanced the impact of IL-1 beta on inflammatory cytokine release and cell apoptosis as quantified using ELISA and flow cytometry. Conversely, ciRS-7 cDNA and miR-7 inhibitor induced the reverse effect. These findings demonstrate that the ciRS-7/miR-7 axis can possibly serve as a regulator in mediating proliferation, apoptosis and inflammation in chondrocytes in the process of OA development.
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