Fig. 4.

miR-30a stimulates proliferator-activated receptor-γ (PPARγ) transactivation in human adipocytes. To validate effects on PPARγ-mediated transcription, human adipocytes were transfected with miR-30a or control mimics, followed by 1 μM rosiglitazone (rosi) treatment for 4 days. A: transcriptional activity was determined by measuring PPAR response element (PPRE)-luc normalized to β-galactosidase (n = 6 independent experiments ± SE; *P < 0.05). Statistical significance was determined by 2-way ANOVA and Tukey post hoc tests. B: the effects of miR-30a overexpression in human adipocytes were characterized by quantitative PCR (qPCR) analysis of adiponectin (ADIPOQ), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), uncoupling protein 1 (UCP1), PPARγ coactivator-1α (PGC1a), iodothyronine deiodinase 2 (Dio2), cell death-inducing DNA fragmentation factor-α (DFFA)-like effector A (CIDEA), and miR-30a-5p (n = 6 independent experiments; *P < 0.05 reflects statistical significance between pairs of measurements). Statistical significance was determined by 2-way ANOVA and Tukey post hoc tests. C: expression levels of CD36, carnitine palmitoyl transferase 1 (CPT1), PPARγ, FABP4, and UCP1 were analyzed by immunoblotting. Human adipocytes were transfected with miR-30a mimics and treated with DMSO [vehicle (veh)] or 1 μM rosiglitazone (rosi) for 4 days. Heat shock protein 90 (HSP90) served as the invariant control.