miR-133a-3p promotes T-2 toxin-induced chondrocyte damage via targeting IGF1R

T-2 toxin is one of the important environmental risk factors of Kashin-Beck disease, which seriously damages cartilage. The present study employed miRNAs to investigate the toxic mechanism of T-2 toxin. In this study, miR-133a-3p was highly expressed in cartilage tissue lesions and chondrocyte damage induced by T-2 toxin. Overexpression of miR-133a-3p promoted T-2 toxin-induced extracellular matrix degradation and apoptosis of chondrocytes. However, inhibition of miR-133a-3p had the opposite effect. These results revealed that miR-133a-3p was involved in regulating T-2 toxin-induced chondrocyte damage. Bioinformatics analysis and dual luciferase assay demonstrated that IGF1R was targeted by miR-133a-3p. The small interfering RNA of IGF1R (Si- IGF1R) promoted T-2 toxin-induced chondrocyte damage. The miR-133a-3p mimics/inhibitor and Si-IGF1R were co-transfected into chondrocytes, and the results showed that the miR-133a-3p mimics strengthened the effect of Si-IGF1R, contrary to the effect of miR-133a-3p inhibitor. In conclusion, miR-133a-3p promoted T-2 toxin-induced chondrocyte damage via targeting IGF1R.