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Plasma levels of matrix metalloproteinase‐8 in patients with carotid atherosclerosis
Author(s) -
Djurić Tamara,
Živković Maja,
Stanković Aleksandra,
Kolaković Ana,
Jekić Djole,
Selaković Vesna,
Alavantić Dragan
Publication year - 2010
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.20393
Subject(s) - matrix metalloproteinase 9 , matrix metalloproteinase , medicine , cardiology , matrix (chemical analysis) , matrix metalloproteinase 3 , chemistry , chromatography
Matrix metalloproteinases (MMPs) are involved in the remodeling of the extracellular matrix (ECM) in the arterial wall during atherogenesis. Collagens are the most abundant proteins in the ECM. MMP‐8 is expressed by cells associated with the development of the atherosclerotic plaque. It cleaves collagen type I three times more potently than two other interstitial collagenases MMP‐1 and MMP‐13. The aim of this study was to investigate whether plasma MMP‐8 values are associated with occurrence of carotid plaque (CP) and possible correlations with clinical and biochemical parameters in carotid atherosclerosis (CA) patients. Total plasma MMP‐8 levels were quantified by ELISA in 63 patients with ultrasonographic evidence of CP presence and 12 controls. Plasma MMP‐8 values were significantly higher in patients with CA compared with controls (median 23.36 ng/ml vs. 13.02 ng/ml, P <0.001) but they did not differ significantly according to gender, smoking and hypertensive status, associated diseases, and use of statins. Statistically significant positive correlations were observed between MMP‐8 plasma values and C reactive protein ( r =0.41, P =0.001), urea ( r =0.50, P <0.001), aspartate transaminase ( r =0.48, P =0.001), and creatinine levels ( r =0.38, P =0.006). These results suggest association of MMP‐8 plasma levels with occurrence of CP and correlation with certain biochemical markers. J. Clin. Lab. Anal. 24:246–251, 2010. © 2010 Wiley‐Liss, Inc.

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