Autologous bone marrow-derived mononuclear cell therapy prevents the damage of viable myocardium and improves rat heart function following acute anterior myocardial infarction.

BACKGROUND We examined the effects of bone marrow-derived mononuclear cells (BMDMNCs) on preventing viable myocardium damage from myocardial infarction (MI) in a rat MI model. METHODS AND RESULTS Saline (group 1) or BMDMNCs (group 2) were implanted into the infarct area (IA) of 1-week-old anterior wall MI Sprague-Dawley (SD) rats. Twenty SD rats without MI served as the controls (group 3). The results demonstrated that in remote viable myocardium, the integrated area (microm2) of connexin43 spots was lower, whereas the number of apoptotic nuclei were higher in group 1 than in groups 2 and 3 on day 90 following BMDMNC implantation (all p<0.001). Additionally, the number of vessels and survival myocardium in the IA was lower in group 1 than in groups 2 and 3 (all p<0.005). Furthermore, the mRNA expressions of nitric oxide synthase, interleukin-8/Gro-alpha, interleukin-10 and matrix metalloproteinase-9 were higher in group 2 than in groups 1 and 3 in peri-IA (all p<0.05). On days 42 and 90, the left ventricular (LV) function was lower in group 1 than in groups 2 and 3 (p<0.001). CONCLUSIONS Autologous BMDMNC therapy improves LV function, and mitigates molecular and cellular perturbation following MI.