Document Detail

Relation of matrix metalloproteinase-9/tissue inhibitor of metalloproteinase-1 ratio in peripheral circulating CD14+ monocytes to progression of coronary artery disease.
MedLine Citation:
PMID:  20152234     Owner:  NLM     Status:  MEDLINE    
Atherosclerosis is an inflammatory disease in which systemic inflammation correlates with disease activity. Matrix metalloproteinases (MMPs) contribute to collagen breakdown in atherosclerotic plaques. In the present study, we investigated whether the ratio of MMP-9 and its endogenous inhibitor, tissue inhibitor of metalloproteinase (TIMP)-1, in circulating monocytes correlates with the clinical stages of coronary artery disease. We studied 18 patients with stable angina pectoris (SAP), 14 patients with unstable angina pectoris and non-ST-segment elevation myocardial infarction (UAP/NSTEMI), 14 patients with ST-elevation myocardial infarction (STEMI), and 16 healthy controls. The protein and mRNA levels of MMP-9 and TIMP-1 in CD14+ monocytes were analyzed using real-time polymerase chain reaction and enzyme-linked immunosorbent assay. The activity of serum MMP-9 was assessed using zymography. Compared to the controls (0.07 +/- 0.01 relative units) and patients with SAP (0.25 +/- 0.1 relative units, p = NS), the monocytic MMP-9 mRNA levels were increased in those with UAP/NSTEMI (0.9 +/- 0.3 relative units, p <0.05 vs SAP) or STEMI (1.6 +/- 0.4 relative units, p <0.05 vs UAP/NSTEMI). In contrast, the protein and mRNA expression of monocytic TIMP-1 levels was 4.5- to 4.7-fold lower in patients with STEMI than in the controls or those with SAP or UAP/NSTEMI (p <0.05). Changes in monocytic expression of MMP-9 and TIMP-1 tracked with the serum levels of MMP-9 and TIMP-1. The activity of serum MMP-9 correlated with the individual MMP-9/TIMP-1 ratio in the peripheral circulating monocytes (r(2) = 0.82, p <0.02). In conclusion, the progression of coronary artery disease was mirrored by an increasing MMP-9/TIMP-1 ratio in the peripheral circulating CD14+ monocytes and serum, respectively. Circulating monocytes displayed the same pattern of imbalance in the expression of MMP-9 and TIMP-1 as previously reported for monocyte-derived macrophages within atherosclerotic plaques, supporting the notion of atherosclerosis as a systemic inflammatory disease.
Stefan Brunner; Jong-Oh Kim; Heiko Methe
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Publication Detail:
Type:  Journal Article     Date:  2010-01-05
Journal Detail:
Title:  The American journal of cardiology     Volume:  105     ISSN:  1879-1913     ISO Abbreviation:  Am. J. Cardiol.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-15     Completed Date:  2010-03-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0207277     Medline TA:  Am J Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  429-34     Citation Subset:  AIM; IM    
Copyright Information:
Copyright 2010 Elsevier Inc. All rights reserved.
Department of Internal Medicine/Cardiology, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany.
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MeSH Terms
Angina Pectoris / blood
Angina, Unstable / blood
Antigens, CD14 / blood*
Biological Markers / blood
Case-Control Studies
Coronary Artery Disease / blood*,  diagnosis,  enzymology
Disease Progression
Enzyme-Linked Immunosorbent Assay
Matrix Metalloproteinase 9 / blood*
Middle Aged
Myocardial Infarction / blood
Myocardium / metabolism
Polymerase Chain Reaction
Sensitivity and Specificity
Severity of Illness Index
Tissue Inhibitor of Metalloproteinase-1 / blood*
Reg. No./Substance:
0/Antigens, CD14; 0/Biological Markers; 0/Tissue Inhibitor of Metalloproteinase-1; EC Metalloproteinase 9

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