(A) Representative M-mode echocardiographic images in Kit^+/+, Kit^W/Kit^W–v, and Kit^W/Kit^W–v mice whose bone marrow was rescued by Kit^+/+ bone marrow after lethal irradiation (Kit^+/+ → Kit^W/Kit^W–v) and Kit^+/+ mice who received the same dose of irradiation and whose bone marrow was reconstituted from other Kit^+/+ mice (Kit^+/+ → Kit^+/+), showing the prevention of ventricular dilation in Kit^+/+ → Kit^W/Kit^W–v mice. (B) Quantification of echocardiographic parameters: left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), fractional shortening (FS), and fractional area contraction (FAC). n =5 per group. Bone marrow rescue prevented ventricular dilation and better preserved ventricular systolic function. (C) Invasive hemodynamic measurements 2 weeks after coronary ligation. Bone marrow rescue also rescued parameters of systolic function, such as ejection fraction and dP/dt maximum (max), and prevented ventricular dilation, but did not affect dP/dt minimum (min). n =5–7 per group. *P <0.05 versus Kit^+/+; **P <0.05 versus Kit^W/Kit^W–v. (D) Bone marrow rescue results in higher myocardial VEGF levels and greater cell cycle activity (PCNA expression). The immunoblots are representative of 4 independent experiments. (E) Quantification of myocardial VEGF from 4 independent experiments performed in triplicate. (F) Bone marrow rescue increases border-zone blood vessels. n =5–7 per group. *P <0.05 versus Kit^W/Kit^W–v (E and F).(G) Recruitment of c-kit⁺ cells from the bone marrow to the injured region of the heart is cardioprotective because it regulates the myocardial balance of angiogenic cytokines.