miR-101 Promotes Degradation of Cartilage Matrix in Osteoarthritis

Abstract

Abnormal GSK-3β or miR-101 expression is associated with osteoarthritis (OA). This study assessed whether miR-101 regulates GSK-3β expression in OA. The cartilage tissue of OA patients and normal cartilage tissue after traumatic amputation were collected to measure miR-101, GSK-3β and β-catenin level. The OA model rats were assigned into OA+antagomiR-NC group and OA+miR-antagomiR-101 group, followed by analysis of Hyp level by ELISA, caspase-3 activity, cell apoptosis by TUENL, as well as the level of miR-101, GSK-3β, β-catenin and COL2A1. miR-101 and β-catenin expression in cartilage tissue of OA was significantly increased and GSK-3β was decreased. miR-101 targeted GSK-3β. OA group showed significantly increased miR-101 and β-catenin level and decreased GSK-3β and COL2A1 level along with increased apoptosis of cartilage tissue. Compared with OA+antagomiR-NC group, miR-101 and β-catenin expression, caspase-3 activity and cell apoptosis in OA+miR-antagomiR-101 group was decreased and GSK-3β and COL2A1 expression was elevated with decreased Hyp content. In conclusion, increased miR-101 expression can reduce GSK-3β expression, enhance Wnt/β-catenin signaling, promote the degradation and destruction of cartilage matrix and play a role in OA pathogenesis. However, inhibition of miR-101 expression can ameliorate OA.