Skip to main content
. 2020 Aug 14;11(8):620. doi: 10.1038/s41419-020-02876-1

Fig. 3. MiR-382 promotes renal fibrosis via PTEN-mediated AKT signaling in AA reduced AKI to CKD.

Fig. 3

a Representative image of immunohistochemical staining for PTEN of human renal biopsy specimens from patients with IgAN with or without tubulointerstitial fibrosis. b Relative expression of miR-382 in human renal biopsy tissues. n = 6 per group. c–g miR-382 suppressed PTEN and activated AKT signaling pathway. Representative and quantification immunoblot analysis of PTEN, AKT, p-AKT Ser473, and p-AKT Thr308 in time course study of SAAN. GAPDH served as standard of PTEN; AKT served as standard of p-AKT; n-6 per group. h The targetScan bioinformatics website was used to predict the possible sequence of PTEN 3′UTR combined with miR-382. Mutation was induced in the PTEN 3′UTR sequence. i luciferase activity was quantified in 293 T cells between the Control group, NC+pMIR-PTEN-plasmid group, miR-382 mimic+ pMIR-PTEN-plasmid group, NC+pMIR− PTEN-mut plasmid group and miR-382 mimic+pMIR-PTEN− mut plasmid group. Dual-luciferase activity was measured via a Dual-Glo Luciferase Assay System. n = 3 per group. j–m Representative and quantification immunoblot analysis of PTEN, AKT, p-AKT Ser473, and p-AKT Thr308 in mice renal from miR-382 WT or KO mice 14 d following severe administering of AA. GAPDH served as standard of PTEN; AKT served as standard of p-AKT; n-6 per group. *P < 0.05; **P < 0.01; ANOVA.