Fig. 2.

Combined deletion of Gata4 and Gata6 in activated cardiac fibroblasts aggravates heart failure after short- and long-term pressure overload. a, b Western blot of isolated cardiac fibroblasts from Gata4/6fl-Per-Cre and Gata4/6fl littermate control mice after pressure overload or sham (a) and quantification of relative protein levels normalized to GAPDH (b) showing efficient reduction of GATA-4 and GATA-6 protein levels after TAC in Gata4/6fl-Per-Cre mice. c–e Quantification of the ejection fraction (c), heart weight/tibia length ratio (HW/TL, d) and lung weight/tibia length ratio (LW/TL, e) in Gata4fl-Per-Cre and Gata4fl littermate control mice shows signs of compensated cardiac hypertrophy without significant differences in both groups after short-term pressure overload. f–h Quantification of the ejection fraction (f), HW/TL (g), and LW/TL ratio (h) in Gata6fl-Per-Cre and Gata6fl littermate control mice shows decreased cardiac function without significant differences in both groups after short-term pressure overload. i–n Quantification of the ejection fraction (i, l), HW/TL (j, m), and LW/TL ratio (k, n) in Gata4/6fl-Per-Cre mice and Gata4/6fl littermate controls shows that mice with deletion of Gata4 and Gata6 in cardiac fibroblasts display a significantly worse cardiac function after short- and long-term pressure overload and an increased LW/TL ratio after long-term pressure overload compared to littermate control mice, while the HW/TL ratio is not significantly different. Selected animals for further histological analysis (see Fig. 3) are indicated in pink. Data are shown as mean ± SD. Two-way ANOVA with Sidak’s multiple-comparisons test was used to test for statistical significance. n.s. indicates no statistical significance between groups. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001