Fig. 5

High glucose induced upregulation of PRMT1 is mediated by miR-574-3p. A RT-qPCR analyzing the miR-574-3p expression in MIN6 cells exposed to high glucose at 6, 12, and 24 h post treatment. *P < 0.05, **P < 0.001, vs. Control; B RT-qPCR analyzing the miR-574-3p expression in MIN6 cells exposed to high glucose (5.5, 16.7, 25, and 33.3 mM) at 2 h post treatment. *P < 0.05, **P < 0.001, vs. 5.5 mM. C PRMT1 was knocked down in MIN6 cells together with miR-574-3p silencing. Cell proliferation was examined by CCK8 assays after high glucose exposure. D PRMT1 was knocked down in MIN6 cells together with miR-574-3p silencing. The cell apoptosis was assessed by flow cytometry after high glucose exposure. E PRMT1 was knocked down in MIN6 cells together with miR-574-3p silencing. The cell AGE levels were determined using an AGEs assay kit. F PRMT1 was knocked down in MIN6 cells together with miR-574-3p silencing. Cell production of ROS was detected utilizing CM-DCF fluorescence. G PRMT1 was knocked down in MIN6 cells together with miR-574-3p silencing. Insulin secretion was determined by ELISA. (H) PRMT1 was knocked down in MIN6 cells together with miR-574-3p silencing. The cell GLUT1 level was examined by RT-qPCR. *P < 0.05, **P < 0.001, vs. 5.5 mM; *P < 0.05, **P < 0.001,, vs. si-NC; ^#P < 0.05, ^##P < 0.001, vs. inhibitor NC; ^&P < 0.05, ^&& P < 0.001, vs. mix