The role of S100A8/A9 in cardiac rupture after myocardial infarction

S100A8/A9 signaling pathway is believed to be related with inflammation. Study found elevated S100A9/ A9 level in patients with acute cardiac infarction. Due to the involvement of acute inflammation of cardiac tissues in the heart rupture after cardiac infarction, this study investigated the role of S100A8/A9 in cardiac rupture. Mouse model with cardiac infarction was established. Recombinant lentiviral vector over-expressing or interfering S100A8/A9 was injected into cardiac tissues. The morality rate of mice was observed within 1 week, along with the detection of myeloperoxidase ( MPO) expression in cardiac tissues by immunohistochemical staining. Over-expression of S100A8/A9 effectively increased the mortality rate of model mice, while RNA interference against S100A8/A9 significantly decreased the mortality rate. Post-mortal examination revealed a positive correlation between cardiac rupture incidence and S100A8/A9 level, which was also directly correlated with MPO expression after cardiac infarction. Inhibition of S100A8/A9 can effectively reduce the inflammatory response after cardiac infarction. In conclusion, S100A8/A9 may enhance the incidence of heart rupture after myocardial infarction via facilitating inflammatory response.