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. 2016 Jun 24;7(30):47760–47776. doi: 10.18632/oncotarget.10283

Figure 2. MiR-27a promotes PPARγ-induced fibrosis in high glucose cultured NRK-52E cells.

Figure 2

(A) MiR-27ai increased PPARγ expression but decreased TGF-β1 (immunofluorescence, scale bar 50 μm) and (B) quantification analysis. (C) MiR-27ai increased the expression of PPARγ but decreased TGF-β1, Smad3, CTGF, Fibronectin, and Collagen I by qRT-PCR and (D) Western blot analyses. (E) MiR-27am decreased PPARγ expression but increased TGF-β1 (immunofluorescence, scale bar 50 μm) and (F) quantification analysis. (G) MiR-27am decreased the expression of PPARγ but increased TGF-β1, Smad3, CTGF, Fibronectin, and Collagen I by qRT-PCR and (H) Western blot analysis. Results are presented as mean ± SD of three independent experiments. *P < 0.05; #P < 0.001. MiR-iNC: miRNA inhibitor negative control; miR-27ai: miR-27a inhibitor; miR-NC: miRNA negative control; miR-27am: miR-27a mimic; p-SMAD3, phospho-SMAD3; t-SMAD3, total-SMAD3. (n = 6).