International Journal of Medical Laboratory
Shahid Sadoughi University of Medical Sciences
Wed, Apr 29, 2026
[Archive]
Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences and Isfahan Pharmaceutical Sciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
Abstract: (47 Views)
Introduction: Acute coronary syndrome (ACS) represents a critical cardiovascular disease. The primary cause of ACS is typically a thrombus (blood clot) forming within a coronary artery at the site of a vulnerable atherosclerotic plaque. Both miRNA-126 (miR-126) and matrix metalloproteinase-2 (MMP-2) are involved in plaque instability and probably related to ACS.
Materials and Methods: Based on the results of angiography and electrocardiography, 46 individuals diagnosed with ACS and 46 patients with stable coronary artery disease (CAD) were enrolled in this study. Gene expression of serum miR-126 was measured using quantitative real-time polymerase chain reaction. Serum total MMP-2 was determined using enzyme-linked immunosorbent assay kit. MMP-2 enzymatic activity was measured through gelatin zymography. The correlation between miR-126 expression and MMP-2 levels was analyzed using the Pearson's bivariate correlation analysis.
Results: The miR-126 level in ACS patients was significantly lower compared to that in the stable CAD group, (p<0.05). In contrast, the serum concentration of MMP-2 was significantly higher in the ACS group (617.3 ng/ml) relative to the stable CAD group (477.1 ng/ml) (p<0.05). Similarrly, MMP-2 activity in serum was significantly higher in ACS patients (3700.1 ± 97 units) than in patients with stable CAD (1912.2 ± 31 unit) (p<0.05). A significant inverse correlation was observed between the expression of miR-126 and serum levels of MMP-2, (r= -0.21, p<0.05).
Conclusion: The findings of this study suggest that miR-126 and MMP-2 may contribute to ACS pathogenesis mechanisms related to coronary plaque instability.
Materials and Methods: Based on the results of angiography and electrocardiography, 46 individuals diagnosed with ACS and 46 patients with stable coronary artery disease (CAD) were enrolled in this study. Gene expression of serum miR-126 was measured using quantitative real-time polymerase chain reaction. Serum total MMP-2 was determined using enzyme-linked immunosorbent assay kit. MMP-2 enzymatic activity was measured through gelatin zymography. The correlation between miR-126 expression and MMP-2 levels was analyzed using the Pearson's bivariate correlation analysis.
Results: The miR-126 level in ACS patients was significantly lower compared to that in the stable CAD group, (p<0.05). In contrast, the serum concentration of MMP-2 was significantly higher in the ACS group (617.3 ng/ml) relative to the stable CAD group (477.1 ng/ml) (p<0.05). Similarrly, MMP-2 activity in serum was significantly higher in ACS patients (3700.1 ± 97 units) than in patients with stable CAD (1912.2 ± 31 unit) (p<0.05). A significant inverse correlation was observed between the expression of miR-126 and serum levels of MMP-2, (r= -0.21, p<0.05).
Conclusion: The findings of this study suggest that miR-126 and MMP-2 may contribute to ACS pathogenesis mechanisms related to coronary plaque instability.
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