ZBTB20 triggerring PI3K/AKT-NF-kappaB signaling requires the suppression of Pten. ZBTB20 triggerring PI3K/AKT-NF-kappaB signaling requires the suppression of Pten

Better understanding of the early molecular events and underlying mechanism will benefit the early-stage diagnose and clinical therapy of OA. In this study, we demonstrated the functions of ZBTB20 in OA pathogenesis via regulating ECM homeostasis. Chondrocytes-specific depletion of Zbtb20 in adult mice attenuated DMM-induced OA progress, restored the balance of ECM anabolism and catabolism. To investigate the underlying mechanism of ZBTB20 in OA progress, RNA-seq was carried out using cultured primary chondrocytes from control and Zbtb20-cKO mice, treated by IL-1β. Overall design: To investigate the underlying mechanism of ZBTB20 in OA progress, we performed gene expression profiles analysisusing cultured primary chondrocytes from control and Zbtb20-cKO mice, treated by IL-1β.