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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Expression of profilin-1 in endothelial cells of rats with acute myocardial infarction.
OBJECTIVE: To analyze the expression of profilin-1 in endothelial cells of rats with acute myocardial infarction.
MATERIALS AND METHODS: Twenty adult male Wistar rats were randomly divided into the myocardial infarction (model) group (n=10) and sham-operation (control) group (n=10). The expression of profilin-1 and phosphorylated extracellular signal kinase (pERK1/2) in aortic endothelial cells, indexes of endothelial injury [levels of endothelial microparticles (EMPs) and nitric oxide (NO)], indexes of myocardial injury [cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB)], and mRNA levels of myocardial apoptotic factors (P53, Fas, Bax, and Bcl-2) in rats between the two groups were compared.
RESULTS: The expression of profilin-1 and pERK1/2 in aortic endothelial cells of rats in the model group was higher than in the control group (p<0.05), the levels of EMPs were increased, and NO levels were lower (p<0.05); cTnT and CK-MB in myocardial tissue, and mRNA of pro-apoptotic factors (P53, Fas, and Bax) were increased, whereas Bcl-2 mRNA was decreased (p<0.05). The protein expression of profilin-1 and pERK1 was positively correlated with the levels of cTnT, CK-MB, EMP, P53, Fas, and Bax, and negatively correlated with the levels of NO and Bcl-2 (p<0.05).
CONCLUSIONS: The high expression of profilin-1 is an important mechanism of acute myocardial infarction, and is expected to become a new target for the treatment of myocardial infarction.
MATERIALS AND METHODS: Twenty adult male Wistar rats were randomly divided into the myocardial infarction (model) group (n=10) and sham-operation (control) group (n=10). The expression of profilin-1 and phosphorylated extracellular signal kinase (pERK1/2) in aortic endothelial cells, indexes of endothelial injury [levels of endothelial microparticles (EMPs) and nitric oxide (NO)], indexes of myocardial injury [cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB)], and mRNA levels of myocardial apoptotic factors (P53, Fas, Bax, and Bcl-2) in rats between the two groups were compared.
RESULTS: The expression of profilin-1 and pERK1/2 in aortic endothelial cells of rats in the model group was higher than in the control group (p<0.05), the levels of EMPs were increased, and NO levels were lower (p<0.05); cTnT and CK-MB in myocardial tissue, and mRNA of pro-apoptotic factors (P53, Fas, and Bax) were increased, whereas Bcl-2 mRNA was decreased (p<0.05). The protein expression of profilin-1 and pERK1 was positively correlated with the levels of cTnT, CK-MB, EMP, P53, Fas, and Bax, and negatively correlated with the levels of NO and Bcl-2 (p<0.05).
CONCLUSIONS: The high expression of profilin-1 is an important mechanism of acute myocardial infarction, and is expected to become a new target for the treatment of myocardial infarction.
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