In summary, MMP-9 mRNA expression is enhanced in monocytes from HD and CAPD patients, and the enhancement may be, in part, associated with cardiovascular complications, including atherosclerosis, in dialysis patients.
This study tested the hypothesis that sequence variation in the promoter region of the gelatinase B gene influences its expression, predisposing individuals carrying certain genetic variants to more severe atherosclerosis.
However, the severity of atherosclerosis in coronary artery or in stent restenosis was not related to any polymorphism of stromelysin-1 or gelatinase B.
In this study we tested the hypothesis that variation in the matrix metalloproteinase-9 gene influences the development of atherosclerosis.Three common polymorphisms, i.e.
The joint action of two susceptibility loci, rather than single MMP genes alone, and the particular combination of MMP3 and MMP9 genotypes present at these loci may contribute to heterogeneity in the presentation of atherosclerosis.
Herein we review the involvement of MMP-9 in a variety of autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, systemic sclerosis, rheumatoid arthritis, multiple sclerosis, polymyositis and atherosclerosis.
Our results suggest that the expression of CD40 and CD40L in the blood cells and the activities of MMP-2 and MMP-9 in plasma were higher in As group than those in Normal group, indicating that they may contribute to the formation of atherosclerosis.
Plasma MMP-9 levels were related neither to MMP-9 PM nor to plaque type, and were related to gender and extension of atherosclerosis in carotid arteries.
Role of proinflammatory alleles in longevity and atherosclerosis: results of studies performed on -1562C/TMMP-9 in centenarians and myocardial infarction patients from Sicily.
We developed a molecular probe of which uptake into cells is synergistically activated by scavenger receptor class A type I (SR-AI) and matrix metalloproteinase-9 (MMP-9), which are the marker receptor and the marker protease of atherosclerosis, respectively.
The serum levels of matrix metalloproteinase (MMP)-3 and -9 are significantly elevated in KD patients, and polymorphisms in the genes encoding MMP-3 and MMP-9 have been associated with the susceptibility, severity, and progression of atherosclerosis and aneurysm.
MMP-9 (matrix metalloproteinase-9), a marker of atherosclerosis previously reported to be associated with NADPH oxidase overactivity, was quantified by ELISA in plasma samples.
The functional genetic polymorphisms present in the promoters of stromelysin-1 (MMP3) and gelatinase B (MMP9) have been shown to be associated with angiographically measured atherosclerosis; however, haplotype analysis of the genetic polymorphisms occurring in the promoters and coding regions of MMP3 and MMP9 has been infrequently performed in the past.
Therefore, in the present study we tried to explore the role of CRP as a possible mediator of atherosclerosis by determining its effect on PPAR-gamma and its effector genes, i.e., liver X receptor-alpha (LXR-alpha) and matrix metalloproteinase-9 (MMP-9) in THP-1 cells.
Cholestin reduces TNF-α-stimulated MMP-2 and MMP-9 expression as well as downregulating NF-κB activation and intracellular ROS formation in HASMCs, supporting the notion that the natural compound Cholestin may have potential application in clinical atherosclerosis disease.
The present study aims to ascertain the polymorphic variants of the MMP-9 gene promoter and its serum levels, which contribute to interindividual differences in susceptibility to atherosclerosis.
Hypertension-induced atherosclerosis was associated with significantly increased levels of MMP-9 mRNA, which may enhance both the deposition of types I and III collagen and atherosclerotic plaque formation.
Serum levels and polymorphisms of matrix metalloproteinases (MMPs) in carotid artery atherosclerosis: higher MMP-9 levels are associated with plaque vulnerability.
In the present study, we investigated the expression of matrix metalloproteinase-9 (MMP-9), which is one of key mediators of atherosclerosis progression, in oxLDL-treated human umbilical vein endothelial cells (HUVEC)-C cells.