Research Paper Volume 11, Issue 18 pp 7510—7524
MiR-27a promotes insulin resistance and mediates glucose metabolism by targeting PPAR-γ-mediated PI3K/AKT signaling
Figure 3. miR-27a targeted at the 3′-UTR of PPAR-γ. In the obese mouse model (A) and IR cells (B), the PPAR-γ expression levels were studied using qPCR. (C) A binding site of miR-27a was found in the 3′-UTR of PPAR-γ mRNA, as evidenced by performing bio-informatic analysis results. (D) After the co-transfection, one from PPAR-γ to a luciferase reporter containing a wild type (WT) or mutant (MU) 3′-UTR, and the other from agomiR-27a into HEK293T cells, a dual-luciferase reporter assay was performed. Effects agomiR-27a transfection on the luciferase activities of the WT (E) and MU (F) PPAR-γ reporter constructs were determined. At both the protein and mRNA levels, a sharp increase was observed for the levels of PPAR-γ in the pancreas of HFD-fed mice after injection with AD-miR-27a, when compared with those of the control animals. WB (G) and qPCR assay (H) showed that miR-27a downregulation obviously increased the expression of both PPAR-γ protein and mRNA. Number of animal per group = 8. **P < 0.01, *P < 0.05, compared to indicated groups.