Fig. 4: Effect of cardiac resident, macrophage-specific ATF3 on cardiac injury and repair after IR.
a, Flow cytometry analysis (left) and quantification (right) of MerTK+, Trem2+, Lyve1+ and MHCII+ macrophages from the heart of ATF3fl/flCx3cr1-Cre− and ATF3fl/flCx3cr1-Cre+ mice 6 h after IR (n = 6 mice per group). b, Representative images of Evans Blue and 2,3,5-triphenyltetrazolium chloride staining in the heart of mice with two genotypes 1 d after IR. Infarct size was calculated as a percentage of the myocardial area at risk (n = 6 mice per group). c, Representative images (left) and quantification (right) of TUNEL+α-actinin+ cardiomyocytes in the heart of mice with the two genotypes 1 d after IR (n = 6 mice per group). Scale bars, 50 μm. d, Flow cytometry analysis (left) and quantification (right) of CD45−PDGFRα−CD31+ ECs in the hearts of mice with the two genotypes (n = 6 mice per group). e,f, Representative IF images (e) and quantification (f) of CD31+ cells in the cardiac border area of mice with the two genotypes (n = 6 mice per group). Scale bars, 20 μm. g, Representative images (left) and quantification (right) of Microfil vascular casting and micro-CT in the hearts of mice with the two genotypes 7 d after IR (n = 6 mice per group). Scale bars, 1 mm. h, Representative echocardiographic images (left) and EF (right) of mice with the two genotypes 30 d after IR (n = 6 mice per group). i, Representative images (left) and quantification (right) of cardiac fibrosis of mice with the two genotypes 30 d after IR (n = 6 mice per group). Scale bar, 1 mm. Statistical significance was evaluated using two-tailed, unpaired Student’s t-test (a) and two-way ANOVA followed by Tukey’s multiple-comparison test (b–d and f–i). All data are presented as mean ± s.e.m.
