Fig. 5.

MiR-199-3p alleviates inflammatory response of OA chondrocytes and stimulates autophagy via targeting TCF4. A Bioinformatics website predicted the binding site between miR-199-3p and TCF4; B The luciferase activity assay verified the targeting relationship between miR-199-3p and TCF4. The results show that Chondrocytes co-transfected with TCF4-WT and miR-199-3p mimic showed decreased luciferase activity; C–E RT-qPCR and Western blot detected TCF4 mRNA and protein expression. After upregulation of miR-199-3p, the expression of TCF4 mRNA and protein decreased; F MTT measured cell proliferation. Upregulation of miR-199-3p promoted chondrocyte proliferation. However, upregulation of TCF4 can weaken the promoting effect of upregulation of miR-199-3p on cell proliferation; G Flow cytometry detected cell apoptosis. Upregulation of miR-199-3p inhibited cell apoptosis. Upregulation of TCF4 can weaken the inhibitory effect of upregulation of miR-199-3p on apoptosis; H ELISA detected contents of pro-inflammatory cytokines IL-1β, TNF-α, IL-6 in the supernatant. Upregulation of miR-199-3p reduced the contents of IL-1β, TNF-α, and IL-6. Upregulation of TCF4 can reduce the effect of upregulation of miR-199-3p; I–J Western blot measured autophagy-correlated Beclin1 and LC3-II/LC3-I ratio. Upregulation of miR-199-3p reduced Beclin1 and LC3-II/LC3-I ratios. Upregulation of TCF4 can reduce the effect of upregulation of miR-199-3p. * P < 0.05, ** P < 0.01. N = 3