Figure 3.

Depressed cardiac function after MI in Cpa3^cre/+ MC-deficient mice. (A) Representative flow cytometry gating of c-kit⁺FcεRI⁺ cells in WT that are absent in Cpa3^cre/+ mice at day 7 after MI (top); bar graphs show the numbers of mature MCs/gram of cardiac tissue (bottom; n = 5–8, two independent experiments). (B) Representative cardiac TB staining (top) and quantitative evaluation of mature MCs in infarcted heart (n = 5–6, two independent experiments). Arrows point to representative cardiac MCs. (C) Left ventricular %SF, LVIDd (left ventricular internal end-diastolic diameter), and LVIDs (left ventricular internal end-systolic diameter) measurements showing significant reduction of cardiac function (day 14) in Cpa3^cre/+ infarcted mice compared with WT (Cpa3^+/+) infarcted mice, with no differences on basal heart function (n = 6–7, two independent experiments). *, P < 0.05; **, P < 0.01, Kruskal–Wallis and Dunn’s post hoc test for comparisons between groups. (D) Cardiac fibrosis, infarct size, capillaries’ density, percentage of cell apoptosis, cardiomyocyte size, and number after infarction (day 14) in WT and Cpa3^cre/+ mice (n = 6–7, two independent experiments). (E) Representative images used for quantification of fibrosis, capillary density, infarct size, and density of apoptotic cardiac cells. Arrows point to representative apoptotic cells. All values are presented as mean ± SEM. Sham, sham-operated animals; WT, Cpa^+/+ littermates.