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. 2017 Mar 9;8(3):e2658. doi: 10.1038/cddis.2017.74

Figure 2.

Figure 2

MiR-27ai attenuates podocyte injury via PPARγ-mediated β-catenin inactivation in high glucose. (a) qRT-PCR analysis shows miR-27ai reduced miR-27a expression in HG cultured podocytes. (b) Representative western blotting shows the expression of phosphorylated and total PPARγ and β-catenin target genes in various conditions as indicated. (c) qRT-PCR analysis shows miR-27ai upregulated the level of PPARγ and podocin but downregulated β-catenin target genes. (d) HG enhanced the interaction of phosphorylated PPARγ and active β-catenin by co-immunoprecipitation. (e) Transwell migration assay and quantitative data show decreased migration of HG cultured podocytes. Scale bar, 100 μm. (f) Wound-healing assay and quantitative data show decreased invasion of HG cultured podocytes. (g) Flow cytometric analysis shows decreased podocyte apoptosis. *P<0.05; #P<0.001. Active β-cat, active β-catenin; 7-AAD, 7-aminoactinomycin D; CTNNB1, catenin beta-1; HG, high glucose; IB, immunoblotting; IP, immunoprecipitation; miR-iNC: miRNA inhibitor negative control; miR-NC: miRNA negative control; NG, normal glucose; PE, phycoerythrin; pPPARγ, phosphorylated peroxisome proliferator-activated receptor γ