Involvement of toll-like receptor 7 (TLR7) in the immune response has been reported in diverse inflammatory diseases. However, the role of TLR7 in the pathogenesis of osteoarthritis (OA) is poorly understood. In this study, we sought to investigate the contribution of TLR7 in regulating chondrocyte apoptosis, inflammation, and degradation of the extracellula matrix (ECM), and its underlying mechanisms. We found that TLR7 expression was increased in cartilage tissues of OA patients and in lipopolysaccharide (LPS)-induced chondrocytes. Silencing of TLR7 alleviated LPS-induced chondrocyte apoptosis, inflammation, and ECM degradation. Mechanistically, TLR7 silencing inhibited the JAK2/STAT3 signaling pathway by inducing p21 expression. Moreover, p21 knockdown and colivein (an activator of JAK2/STAT3 signaling) partially rescued the suppressive role of TLR7 silencing on chondrocyte apoptosis, the inflammatory response, and ECM underproduction. Taken together, our data revealed that knockdown of TLR7 attenuated chondrocyte apoptosis and injury by blocking the p21-mediated JAK2/STAT3 pathway, suggesting that TLR7 may be a therapeutic target in OA.
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