Role of matrix metalloproteinase 1, 2, 3 and 9 in acute myocardial infarction Print

Current evidence indicates that extracellular matrix (ECM) remodeling is a component of acute myocardial infarction (AMI) and matrix metalloproteinase (MMP) has a role in early atherosclerosis, plaque rupture and myocardial infarction (MI). The necessity of inhibition of ECM remodeling and subsequent injuries in patients with AMI suggests that MMP might be involved in this task. Here, we investigated the activities of MMP-1, -2, -3, and -9 which play an important role in AMI.
Plasma and peripheral blood mononuclear cells (PBMCs) of 50 patients with AMI were isolated from peripheral blood after the onset of AMI within 24 h, comparing with 50 control subjects. The active form of MMPs was measured by enzyme linked immunosorbent assay (ELISA); MMP proteins presence and expression by immunoblotting and zymography analysis; and mRNA expression of MMPs by real time reverse transcriptase polymerase chain reaction.
Plasma concentrations of MMPs increased in patients rather than control subjects. Gel zymography revealed 43, 66, 45, and 83 kDa molecular weight bands which was consistent with active MMP-1, -2, -3, and -9, respectively, exhibiting gelatin-degrading activity in both patient and control subjects. No up-regulation of mRNA expression was found out.
To the best of our knowledge, it is the first monitoring of MMP gene and protein expression and also circulating active MMPs in Iranian patients with AMI and normal subjects. Up-regulation of MMPs activity is common in the failing myocardium and missing up-regulation of transcription indicates that protein levels of MMPs were regulated at the post transcriptional level.