Myocardial Tissue In Acute Myocardial Infarction Integrin-linked Kinase Expression Changes

Objective In order to investigate the role of integrin-linked kinase (ILK) during progressive heart dysfunction after acute myocardial infarction (MI), we observed the changes of heart function as well as ILK expression at different time points after myocardial infarction. Methods Left anterior descending arteries of adult male SD rats were ligated to form acute myocardial infarction models. Cardiac function was evaluated by echocardiography and left ventricular catheter. Real time PCR and Western blot were used to assess ILK expression in non-infarct area. VEGF expression and phosphorylation of eNOS in non-infarct area were determined by Western blot. Apoptosis rate of non-ischemic cardiomyocytes was determined by TUNEL assay. The above parameters were examined in different time points after post acute myocardial infaction. Results After MI, heart function was significantly decreased. Lower of dp/dtmax and higher LVEDP of 8 weeks group was observed, compared with 1 and 4 weeks groups post MI. Meanwhile, ILK, VEGF expression and phosphorylation of eNOS in non-infarct area were increased in 1 and 4 weeks groups and decreased significantly in 8 weeks groups post MI. TUNEL assay indicated a higher apoptosis rate of non-infarct cardiomyocytes in 8 weeks group post MI than other groups. Conclusion Although temporary ILK up-expression in non-infarct area post acute myocardial infarction maintains compensatory cardiac function, long-term down-regulation of ILK pathway may finally lead to cardiac decompensation.