Increased levels of oxidative stress and p53, Bax, and Bcl2 gene expression in patients with acute myocardial infarction

Apoptosis is implicated in unfavorable remodeling of the left ventricle during acute myocardial infarction (AMI). Both DNA damage and p53 play important roles in regulating apoptosis. Expression patterns of apoptotic regulating genes such as p53, bax, and bcl-2 highlight the importance of inhibiting ventricle remodeling and subsequent injuries. In the present cohort study, serum levels of p53 and 8hydroxy-2-deoxyguanosine (8-OHdG) as well as p53, bax, and bcl-2 expression were examined after the onset of AMI in Iranian patients. Serum levels of p53 and 8-OHdG were measured by enzyme-linked immunosorbent assay (ELISA) and the presence of p53 protein and mRNA expression of p53, bax, and bcl-2 were analyzed by Western blotting and real time RT-PCR methods, respectively. In patients presenting with AMI, serum levels of p53 and 8-OHdG increased in comparison with healthy controls. Likewise, transcripts of p53 and bax were also elevated in patients, while bcl-2 decreased. Our data suggest the novel use of p53 and 8-OHdG as markers of apoptosis and DNA damage following AMI. Our results also revealed that apoptosis occurs in concert with an up-regulation of p53 and bax and a downregulation of bcl-2 which may suggest a possible therapeutic intervention in patients recovering from AMI.