Fig. 2From: The PPARγ agonist pioglitazone prevents TGF-β induced renal fibrosis by repressing EGR-1 and STAT3Gene and protein expression of fibrosis related molecules. As compared to control mice, the renal mRNA expression of lipocalin-2 (Lcn2) (a), alfa-smooth muscle actin (Acta2) (b), TGF-β1 (Tgfb1) (c) and CTGF (Ctgf) (d) were elevated in untreated TGF-β1 transgenic mice, but reduced to control levels by pioglitazone treatment. The kidneys of untreated TGF-β1 mice depicted significantly more early growth response factor-1 (EGR-1) positive nuclei (e and f, see asterisks), as compared to controls or pioglitazone treated TGF-β1 mice (400x magnification, bar represents 50 μm; insets: 630x magnification). The strong fibrotic response in TGF-β1 kidneys was associated with significant STAT3 phosphorylation (g). Kruskal-Wallis test (n = 7/group), *:p < 0.05, **:p < 0.01, ***:p < 0.001Back to article page