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Increased plasma concentration of matrix metalloproteinase-7 in patients with coronary artery disease
- Nilsson, L (författare)
-
- Jonasson, Lena, 1956- (författare)
- Östergötlands Läns Landsting,Linköpings universitet,Hälsouniversitetet,Kardiologi,Kardiologiska kliniken
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- Nijm, Johnny, 1969- (författare)
- Linköpings universitet,Institutionen för medicin och vård,Hälsouniversitetet
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- (creator_code:org_t)
- 2006-08-01
- 2006
- Engelska.
- Ingår i: Clinical Chemistry. - : Oxford University Press (OUP). - 0009-9147 .- 1530-8561. ; 52:8, s. 1522-1527
- Tidskriftsartikel (refereegranskat)
Abstract
Ämnesord
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- Background: Plaque rupture is often associated with breakdown of the extracellular matrix in the shoulder region of a plaque. We tested whether plasma concentrations of various matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase-1 (TIMP-1) could serve as markers for plaque instability as well as relationships between plasma MMPs and inflammatory markers. Methods: The study group included 65 men with angiographically verified CAD (45 with stable and 20 with unstable CAD) and 28 healthy controls. Circulating MMP, TIMP-1, C-reactive protein, and cytokine concentrations were measured by ELISA. Leukocyte subtype counts in whole blood were determined, and T-cell subsets and natural killer cells were measured by flow cytometry. Differences in continuous variables between groups were tested by ANOVA with the Scheffé F-test used as a post hoc test, and correlations were analyzed by a linear regression method. Results: The plasma concentration of MMP-7 was increased in patients with stable and unstable CAD, whereas MMP-2 and -3 concentrations were decreased. The plasma concentration of TIMP-1 was significantly increased in patients with unstable CAD. MMP-2, -3, and -7 showed no correlations with established markers of inflammation. However, MMP-2 correlated positively with the number of natural killer cells in patients with stable and unstable CAD. Conclusion: Plasma concentrations of MMPs and TIMPs may be markers of CAD but appear to be differentially regulated. © 2006 American Association for Clinical Chemistry.
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