#5503 PIOGLITAZONE REVERSES MIR-130A AND MIR-199 DYSREGULATION INDUCED BY TGF-BETA DURING KIDNEY FIBROSIS

Abstract Background and Aims The peroxisome proliferator-activated receptor-γ (PPARγ) agonists have been shown to dampen TGF-β signaling suppress miR-130a in VSMCs also profibrotic miR-21-5p the kidney. We recently demonstrated that pioglitazone ameliorates established renal fibrosis by suppressing STAT3 EGR1 [1], but its effect on has not investigated. Thus, we aimed study how chronic oral treatment would affect TGF-β–driven miRNA dysregulation mice. Method Ten week old male C57Bl6 control (CTL, n = 6) transgenic mice (TGFb, 12, having elevated plasma TGF-β1 level) were used. CTL half of TGFb received regular chow. second containing chow (dose: 20mg/kg/day) for 5 weeks (TGFb+Pio, 6), when kidneys evaluated. Results Untreated had a 4.7-fold 2.8-fold type I III collagen mRNA overexpression as compared controls, respectively. This was accompanied 3.8-fold pro-fibrotic Egr2 mRNA, 2.9-fold miR-130a, 3.9-fold miR-199 3.3-fold miR-21 overexpression. Chronic with PPARγ agonist reduced expression both mRNAs miRNAs levels, reached even lower values than kidneys. Interestingly, miR-200a (regulated TGF-beta known ameliorate fibrosis) similar all groups, regardless treatment. Conclusion Our data indicate only attenuates induced overexpression, miR-199, supporting anti-fibrotic effects.