miR-20a regulates inflammatory in osteoarthritis by targeting the IκBβ and regulates NK-κB signaling pathway activation.

In the cartilage and synovial microenvironment of osteoarthritis (OA) patients, utmost changes are commonly brought upon by the inflammatory cytokines, leading to cellular dysfunction, particularly in chondrocytes. The regulation of chondrogenesis, a key part is played the microRNAs. Thus, the current study aimed to assess the function of miR-20a in osteoarthritis. The miR-20a expression was observed to increase in the tissues of OA cartilage, when compared with tissues of normal cartilage, and enhanced proliferation of chondrocyte was observed in the presence of miR-20a. Moreover, on treating the chondrocytes with LPS (lipopolysaccharide), an increase in miR-20a level was observed. On transfecting with miR-20a inhibitor, inhibition in production of LPS-induced pro-inflammatory cytokines as well as cell apoptosis were seen. The assay for luciferase activity showed that the expression of IκBβ was impeded on being targeted at its 3'-UTR by miR-20a. The transfection of IκBβ and inhibitor of miR-20a repressed the NF-κB pathway activation and chondrocyte cellular apoptosis. An OA model was established for in vivo studies on rats by ACLT (anterior cruciate ligament transection). In conclusion, the results demonstrate an increase in articular cavity inflammation in rats with OA in the presence of miR-20a by targeting on IκBβ and activating the NF-κB signaling pathway.

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