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Association of serum MMP-9 with autoantibodies against oxidized LDL
A Kalela1, T A Koivu, M Höyhtyä
1Department of Medical Biochemistry, University of Tampere Medical School, University of Tampere, FIN-33014 Tampere, Finland.
Abstract:
Monocyte-derived macrophages in atherosclerotic plaques secrete matrix metalloproteinases (MMPs), which may contribute to plaque rupture. There has been much speculation as to which factors precipitate in the arterial inflammation. Oxidized low density lipoprotein (oxLDL) has been suggested to have proinflammatory properties, and it has been shown to increase matrix metalloproteinase-9 (MMP-9) secretion by macrophages in vitro. We determined serum MMP-9 concentration and autoantibodies against oxLDL by ELISA in men with angina pectoris (n=243) and age-matched controls (n=238). The association between serum MMP-9 concentration and autoantibodies against oxLDL was evaluated. Autoantibody level against oxLDL, expressed in optical density units, was significantly higher in subjects with angina pectoris compared to controls (0.100+/-0.064 versus 0.088+/-0.051, respectively, P=0.030), but serum levels of MMP-9 did not differ significantly between these groups (54.2+/-29.9 versus 50.6+/-23.1 microg/l). However, autoantibodies against oxLDL correlated positively with serum MMP-9 (r=0.21, P<0.001). In a multiple regression model (including age, diastolic blood pressure, cholesterol, HDL cholesterol, triglycerides, BMI, smoking and MMP-9) serum MMP-9 (beta=0.200, P<0.001) and smoking (beta=0.179, P<0.001) were significantly associated with autoantibodies against oxLDL. In conclusion, autoantibodies against oxLDL were positively associated with angina pectoris and serum MMP-9. Since autoantibody level against oxLDL could be expected to reflect the degree of oxLDL in the vessel wall, our results suggest that oxLDL is associated with MMP-9 in vivo.
Insights
Autoantibodies against oxidized low-density lipoprotein (oxLDL) were higher in men with angina pectoris and correlated with serum matrix metalloproteinase-9 (MMP-9). These findings suggest oxLDL is linked to MMP-9 in vivo, potentially contributing to arterial inflammation.
Area of Science:
- Cardiovascular Research
- Immunology
- Biochemistry
Background:
- Macrophages in atherosclerotic plaques secrete matrix metalloproteinases (MMPs), potentially causing plaque rupture.
- Oxidized low-density lipoprotein (oxLDL) is suspected to promote arterial inflammation and increase MMP-9 secretion by macrophages.
- The relationship between oxLDL, MMP-9, and angina pectoris requires further investigation.
Purpose of the Study:
- To determine serum MMP-9 concentration and autoantibodies against oxLDL in men with angina pectoris and controls.
- To evaluate the association between serum MMP-9 concentration and autoantibodies against oxLDL.
- To explore the in vivo relationship between oxLDL and MMP-9 in the context of cardiovascular disease.
Main Methods:
- Serum MMP-9 concentration and autoantibodies against oxLDL were measured using ELISA in 243 men with angina pectoris and 238 age-matched controls.
- Statistical analyses, including correlation and multiple regression, were employed to assess associations.
- Factors such as age, blood pressure, lipid profile, BMI, and smoking status were included in the regression model.
Main Results:
- Autoantibody levels against oxLDL were significantly higher in subjects with angina pectoris compared to controls (P=0.030).
- Serum MMP-9 levels did not differ significantly between the groups.
- Autoantibodies against oxLDL showed a positive correlation with serum MMP-9 (r=0.21, P<0.001).
- Multiple regression analysis indicated that serum MMP-9 and smoking were significantly associated with autoantibodies against oxLDL (P<0.001 for both).
Conclusions:
- Autoantibodies against oxLDL are positively associated with angina pectoris and serum MMP-9 levels.
- The findings suggest an in vivo association between oxidized low-density lipoprotein and MMP-9.
- This association may play a role in the inflammatory processes underlying atherosclerosis and plaque instability.