circRNA.33186 Contributes to the Pathogenesis of Osteoarthritis by Sponging miR-127-5p
| Autor: | Zhi-bin Zhou, Lei Zhu, Qiang Fu, Gao-xiang Huang, Bin Han, Aimin Chen, Jia-jia Lu |
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| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
Male
Blotting Western Interleukin-1beta Type II collagen Fluorescent Antibody Technique Inflammation Apoptosis Osteoarthritis Pathogenesis 03 medical and health sciences Mice 0302 clinical medicine Downregulation and upregulation Drug Discovery Matrix Metalloproteinase 13 Genetics medicine Gene silencing Animals Molecular Biology Collagen Type II Cells Cultured 030304 developmental biology Cell Proliferation Pharmacology 0303 health sciences Gene knockdown business.industry RNA Circular medicine.disease Immunohistochemistry Mice Inbred C57BL MicroRNAs 030220 oncology & carcinogenesis Cancer research Molecular Medicine Original Article medicine.symptom business |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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