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.
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.
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.
However, the severity of atherosclerosis in coronary artery or in stent restenosis was not related to any polymorphism of stromelysin-1 or gelatinase B.
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.
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 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.
Role of proinflammatory alleles in longevity and atherosclerosis: results of studies performed on -1562C/TMMP-9 in centenarians and myocardial infarction patients from Sicily.
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.
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.
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.
Toll-like receptor 4 (TLR4) and matrix metalloproteinase-9 (MMP-9) are known to play important roles in inflammatory diseases such as arteriosclerosis and plaque instability.
Previously, Matrix metalloproteinase-9 (MMP-9), monocyte chemotactic protein-1 (MCP-1) and toll-like receptor 4 (TLR4) were confirmed to play an important role in atherosclerosis and plaque instability.
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.
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.
Based on the studies performed so far, it is assumed that IL-17 contributes to development of atherosclerosis by means of: stimulation of production of proinflammatory compounds; induction of apoptosis of endothelial cells and heart muscle cells; stimulation of von Willebrand factor production; and induction of the matrix metalloproteinase-9 (atherosclerotic plaque rupture).