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Mol Ther. 2019 Mar 6;27(3):531-541. doi: 10.1016/j.ymthe.2019.01.006. Epub 2019 Jan 15.

circRNA.33186 Contributes to the Pathogenesis of Osteoarthritis by Sponging miR-127-5p.

Author information

1
Department of Orthopaedics, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
2
Department of Pathology, No.924 (No.181) Hospital of People's Liberation Army, Guilin, Guangxi, 541002, China.
3
Department of Orthopaedics, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China. Electronic address: aiminchen@smmu.edu.cn.
4
Department of Orthopaedics, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China. Electronic address: hailangzhulei@smmu.edu.cn.

Abstract

Osteoarthritis (OA), the most prevalent age-related joint disorder, is characterized by chronic inflammation, progressive articular cartilage destruction, and subchondral bone sclerosis. Accumulating evidences indicate that circular RNAs (circRNAs) play a critical role in various diseases, but the function of circRNAs in OA remains largely unknown. Here we showed that circRNA.33186 was significantly upregulated in IL-1β)-treated chondrocytes and in cartilage tissues of a destabilized medial meniscus (DMM)-induced OA mouse model. Knockdown of circRNA.33186 increased anabolic factor (type II collagen) expression and decreased catabolic factor (MMP-13) expression. Knockdown of circRNA.33186 also promoted proliferation and inhibited apoptosis in IL-1β-treated chondrocytes. Silencing of circRNA.33186 in vivo markedly alleviated DMM-induced OA. Mechanistic study showed that circRNA.33186 directly binds to and inhibits miR-127-5p, thereby increasing MMP-13 expression, and contributes to OA pathogenesis. Taken together, our findings demonstrated a fundamental role of circRNA.33186 in OA progression and provide a potential drug target in OA therapy.

KEYWORDS:

circRNA.33186; circular RNAs; miR-127-5p; osteoarthritis

PMID:
30692016
PMCID:
PMC6402950
[Available on 2020-03-06]
DOI:
10.1016/j.ymthe.2019.01.006

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