Allogeneic bone marrow mesenchymal stem cell transplantation for acute myocardial infarction in rats / 中国组织工程研究

ABSTRACT

BACKGROUND:A number of studies have shown that bone marrow mesenchymal stem cells can survive in the infarcted myocardium and improve cardiac function. OBJECTIVE:To investigate the effects of al ogeneic rat bone marrow mesenchymal stem cells on heart failure in acute myocardial infarction models of rats and possible mechanisms. METHODS:Rat bone marrow mesenchymal stem cells were isolated from the bone marrow of 39 male Wistar rats by density gradient centrifugation with Percol . After ligating anterior descending coronary artery, 39 female Wistar rats were randomly divided into three groups:control group (Dulbecco’s modified Eagle’s medium, n=12), mesenchyma stem cells group (n=15) and mononuclear cells group (n=12). Eight weeks later, hemodynamics and left ventricular function were measured. Histopathological and immunohistochemical examinations were performed. RESULTS AND CONCLUSION:Compared with the control group, left ventricular end diastolic pressure, left ventricular relative weight, the col agen volume fraction of type I and type III in the infarction zone of the left ventricle were al significantly decreased, in contrast to ±dp/dtmax,-dp/dtmax/left ventricular systolic pressure, body weight and vascular density in infarction zone were al significantly increased both in mesenchymal stem cells group and mononuclear cells group. There were no significant differences between two treatment groups except for interventricular septal thickness and vascular density in non-infarction zone. 5-Bromo-2'-deoxyuridine positive cells were observed in the infarction area of mesenchyma stem cells group but no positive cells in mononuclear cells group. Some bal-like cellmasses were found positively stained with desmin and cardiac troponin T. Results have suggested that embedded bone marrow mesenchymal stem cells survived in exogenous host hearts. The therapy of mononuclear cells and mesenchymal stem cells could limit the left ventricular remodeling after acute myocardial infarction and improve left ventricular function through angiogenesis inducing and col agen deposition decreasing.