Fig. 2: KDM5B deficiency protects the heart from dysfunction and adverse cardiac remodeling after MI. | Experimental & Molecular Medicine

Fig. 2: KDM5B deficiency protects the heart from dysfunction and adverse cardiac remodeling after MI.

From: Loss of KDM5B ameliorates pathological cardiac fibrosis and dysfunction by epigenetically enhancing ATF3 expression

Fig. 2

a Echocardiographic measurement of the LVEF, LVFS, left ventricular end-diastolic internal dimension (LVIDd), and left ventricular end-systolic internal dimension (LVIDs) of KDM5B-KO or WT mice at baseline (Day 0) and on the indicated day after MI or sham operation (n = 6 mice per group). b–e Representative Masson’s trichrome staining images and quantitation of the scar size (b, c) or Sirius red staining images and quantitation of the fibrosis area (d, e) in myocardial tissues from KDM5B-KO or WT mice on Day 28 after MI. n = 6 mice per group. Scale bar, 1.6 mm (upper), 200 μm (bottom). f Q-PCR analysis of Col1a1 and Col3a1 mRNA levels in myocardial tissues from KDM5B-KO or WT mice on Day 14 after MI or sham operation (n = 6 mice per group). g Representative immunofluorescence staining of α-SMA (red) and Col III (green) in myocardial tissues from KDM5B-KO or WT mice on Day 14 after MI (n = 6 mice per group). Scale bar, 50 μm. *p < 0.05, **p < 0.01, ***p < 0.001. Unpaired Student’s t test (c, e) or ANOVA (a, f) was performed.

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