期刊
MOLECULAR THERAPY
卷 27, 期 3, 页码 531-541出版社
CELL PRESS
DOI: 10.1016/j.ymthe.2019.01.006
关键词
-
资金
- National Natural Science Foundation of China [81571204, 81701215, 81874003]
- Shanghai Sailing Program [17YF1425300]
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 circularRNAs(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-1 beta)-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-1 beta-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 inOAprogression and provide a potential drug target in OA therapy.
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