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Abstract
Osteoarthritis (OA) is a common, degenerative joint disease characterized by articular cartilage degradation. Currently, clinical trials based on microRNA therapy have been performed to treat various diseases. However, no treatment has been found for arthritis. This study investigated the functions of miR-101 in cartilage degradation in vivo and evaluated the feasibility of using miR-101 as a therapeutic agent for OA. Mono-iodoacetate-induced arthritis (MIA) rats were used as an animal model of OA. miR-101 mimic or miR-101 inhibitor was injected into the rats' knees to evaluate its effects on cartilage degradation. Cartilage degradation aggravated at 14 days after the injection of miR-101 mimic. By contrast, miR-101 silencing reduced cartilage degradation. Moreover, the administration of miR-101 mimic is sufficient to cause cartilage degradation in the normal cartilage of rats. By contrast, miR-101 inhibitor could prevent this change. Microarray and qPCR were used to investigate the different expressed genes after injecting miR-101 mimic and miR-101 inhibitor in the rats' articular cartilage. Several cartilage degradation-related genes were selected and validated to function in cartilage degradation with miR-101. Our results demonstrated the therapeutic effect of miR-101 inhibition on cartilage degradation in MIA rats by regulating several cartilage degradation–related genes.
Highlights
Osteoarthritis (OA) is a common degenerative joint disease that causes joint pain, swelling, and even dysfunction
Expression changes in miR-101 and Sox[9] after injecting Ad-miR-101 mimic and inhibitor in the cartilage of Mono-iodoacetate-induced arthritis (MIA) rats To test whether exogenous miR-101 can penetrate into the cartilage, frozen sections of rat knees were examined by confocal microscopy after the injection of green fluorescent protein (GFP)–tagged Ad-miR-101 mimic, Ad-miR-101 inhibitor, or Ad-Scr
Our previous report demonstrated that downregulated miR-101 expression prevented the IL-1β–induced extracellular matrix (ECM) degradation in chondrocytes.[20]
Summary
Osteoarthritis (OA) is a common degenerative joint disease that causes joint pain, swelling, and even dysfunction. The treatment of OA is unsatisfactory: it is only limited to pain management. OA is characterized by structural and biochemical changes in the articular cartilage, including progressive chondrocyte degradation and insufficient synthesis of its extracellular matrix (ECM).[4,5] Cartilage degradation is irreversible and incurable because of its limited capacity for repair. Several molecular mechanisms of cartilage degradation have already been characterized, the currently available information is still limited, and no effective methods can be used for OA prevention or treatment.[6,7,8] further understanding of the molecular mechanism is important to investigate potential therapeutic targets
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