Objective       To determine the effects of adenoviral gene transfer of angiotensin converting 1-7 (Ang-(1-7)) on the ventricular remodeling in rats with acute myocardial infarction (AMI) and investigate the possible protective mechanisms.       Methods       A total of 40 male Sprague-Dawley rats were randomly divided into 4 groups (n=10 for each group)

that is

sham operation group

MI group

AMI+EGFP group and MI+Ang-(1-7) group. AMI model were induced by ligation of the left anterior descending coronary artery. Rats in the MI+EGFP and MI+Ang(1-7) groups received an intra-myocardial injection of EGFP and Ang-(1-7)

respectively. Rats in the MI and sham operation groups received no injection intervention. In 4 weeks later

heart weight/body weight (HW/BW)

left ventricular end diastolic pressure (LVEDP)

dp/dtmax and dp/dtmin were examined. Myocardial structure changes and collagen deposition were evaluated histopathologically. The expression of Ang-(1-7)

MMP-2

TIMP-2

collagen type I and collagen type Ⅲ were measured by Western blotting and immunohistochemical staining.       Results        The protein expression of Ang-(1-7) was significantly higher in myocardial tissue in MI+Ang-(1-7) group than the other groups. Compared with the sham operation group

the expression levels of Ang-(1-7)

MMP-2

TIMP-2

collagen type I and Ⅲ in the tissue around the infarct

and the ratio of collagen type Ⅰ to Ⅲ  were increased

the ratio of ventricular/body weight and LVEDP were significantly higher

and dp/dtmax and dp/dtmin were significantly decreased in MI and MI+EGFP groups. MI+Ang-(1-7) group had significantly increased expression of Ang-(1-7) and TIMP-2

obviously elevated dp/dtmax and dp/dtmin

and markedly decreased MMP-2

collagen type Ⅰ and Ⅲ  the ratio of collagen type Ⅰ to Ⅲ when compared with MI and MI+EGFP group.       Conclusion       Ang-(1-7) significantly improves extracellular matrix remodeling after myocardial infarction

which may be related to up-regulation of TIMP-2 and down-regulation of MMP-2.