Influence of Transplantation of Allogenic Bone Marrow Mononuclear Cells on the Left Ventricular Remodeling of Rat after Acute Myocardial Infarction
- Author:
Ruicheng ZHANG
1
;
Nianguo DONG
;
Jianfeng HOU
;
Xian'en FA
Author Information
1. 华中科技大学同济医学院附属协和医院
- Keywords:
bone marrow mononuclear cell;
cell transplantation;
rat;
acute myocardial infarction;
ventricular remodeling
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2006;26(6):696-699
- CountryChina
- Language:Chinese
-
Abstract:
To probe into the influence of transplantation of allogenic bone marrow mononuclear cells (BM-MNCs) on the left ventricular remodeling of rat after acute myocardial infarction (AMD,60 male Wistar rats were evenly divided into three groups at random: control group 1, control group 2and transplantation group. In control group 1, chest was opened without ligation of coronary artery;in control group 2 and transplantation group, the left anterior descending branch of coronary artery was ligated to establish AMI model. Prepared culture medium and allogenic BM-MNCs suspension were respectively implanted the surrounding area of infracted cardiac muscle via epicardium of control group 2 and transplantation group. Four weeks after the operation, the osteopontin gene (OPN mRNA, P<0.01), type Ⅰ collagen (P<0.01) and angiotensin Ⅱ (AngⅡ, P<0.01) content in the left ventricular non-infracted myocardium, and the Ang Ⅱ density in blood plasma (P<0.05) of transplantation group and control group 2 were all significantly higher than that of control group 1. In the transplantation group, the myocardial OPN mRNA, type Ⅰ collagen and Ang Ⅱ content of non-infracted zone in left ventricle, and the Ang Ⅱ concentration in blood plasma were all significantly lower than those of control group 2 (P<0.05 for all). It is concluded that allogenic BM-MNCs transplantation may ease left ventricular remodeling after AMI by inhibiting the synthesis of type Ⅰ collagen in the cardiac muscle and down-regulating the expression of Ang Ⅱ and OPN gene.