Metalloproteinases in Development and Progression of Vascular Disease

Lijnen, H.R.

doi:10.1159/000083814

Cited by 95 publications

(71 citation statements)

References 80 publications

(65 reference statements)

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“…11 MMP-9 and MMP-2 are highly expressed in the vulnerable regions of atherosclerotic plaque and it has been suggested that they are causally involved in plaque rupture. 22 Other studies have shown that the level of MMP-2 activity is higher in stable lesions of carotid artery plaque, 10 and that the level of MMP-9 is increased in more unstable plaque. 10,20 Our finding that the MMP-9 level was higher in patients with ruptured plaque would support the evidence of an association between plaque vulnerability and MMP-9.…”

Section: Discussionmentioning

confidence: 96%

Relationship Between Multiple Plasma Biomarkers and Vulnerable Plaque Determined by Virtual Histology Intravascular Ultrasound

Park

Lee

Shim

et al. 2010

Circ J

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Background:The relationship between plasma biomarkers and vulnerable plaque is not well understood. Methods and Results:The 188 patients who underwent 3-vessel virtual histology (VH) intravascular ultrasound (IVUS) with peripheral blood sampling were enrolled. Plasma levels of matrix metalloproteinase 2 and 9 (MMP-2, -9), tissue inhibitor of metalloproteinase-1, adiponectin, and macrophage migration inhibitory factor were measured. VH-IVUS-derived thin cap fibroatheroma (VH-TCFA) was defined as a necrotic core >10% of plaque area in the presence of >40% plaque burden. There were 38 patients with ruptured plaque and 150 patients without (107 patients with VH-TCFA, 43 patients without VH-TCFA) in culprit/target lesions. Among the biomarkers, only the MMP-9 level was significantly higher in patients with ruptured plaque (P=0.002). In the subgroup without ruptured plaque, significant differences in the levels of several biomarkers were not observed between patients with and without VH-TCFA. In both culprit/target and nonculprit/non-target vessels, the MMP-9 level showed a weak correlation with the total number of ruptured plaques (r=0.231, P=0.002).Conclusions: Among the biomarkers tested in this study, the MMP-9 level was significantly higher in patients with ruptured plaque. However, measurement of several biomarkers, including MMP-9, was incapable of predicting the presence of VH-TCFA. (Circ J 2010; 74: 332 - 336)

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Section: Discussionmentioning

confidence: 96%

Relationship Between Multiple Plasma Biomarkers and Vulnerable Plaque Determined by Virtual Histology Intravascular Ultrasound

Park

Lee

Shim

et al. 2010

Circ J

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“…[10][11][12] Furthermore, MMP9 is highly expressed in the weak regions of atherosclerotic plaques and may be causally involved in plaque rupture. [13][14][15] The increase in plasma concentrations of MMP9 may be a predictor of cardiovascular disease risk and plasma MMP9…”

Section: Introductionmentioning

confidence: 99%

Association of MMP‐9 gene polymorphisms with nephrolithiasis patients

Mehde

Mehdi

Yusof

et al. 2017

Clinical Laboratory Analysis

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Background Nephrolithiasis is one of the causes which lead to chronic kidney disease (CKD). Matrix metalloproteinases (MMPs) are endopeptidases degrading extracellular matrix which correlate with the pathogenesis of atherosclerosis. The current study was designed to analyze the association of (R279Q, C1562T) polymorphism of MMP‐9 with nephrolithiasis patients. Methods Genotyping of MMP‐9/R279Q and of MMP‐9/C1562T polymorphism were carried out by PCR‐based restriction digestion method. Serum level of MMP‐9, oxidative stress marker, MDA, and uric acid were measured in patients and control. Results Allele frequencies of the MMP‐9/C1562T polymorphism for C and T allele were 71.25% and 28.75% in patients, 87.08% and 12.92% in control respectively. The homozygote TT was more frequent in the nephrolithiasis patients group, while T allele frequency was significantly higher in the nephrolithiasis patients group than in the control group. The patients with CT and TT genotype showed a significant increase in serum MMP‐9, Total Oxidant Status (TOS), Oxidative Stress Index (OSI), Malondialdehyde (MDA), and uric acid when compared to CC genotype in patients with nephrolithiasis. The R279Q polymorphism site with regard to the relationship with nephrolithiasis was not significant. Conclusion The result indicates that patients with TT genotype had an increased risk of stones. Also, the results demonstrate that TT allele of the C1562T polymorphism in the MMP‐9gene is related with an increase of oxidative stress in nephrolithiasis patients and may possibly impose a risk for cardiovascular diseases in patients with TT genotype of MMP‐9.

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“…T-cell populations with different functional capacities have been identified within atherosclerotic lesions [4] and contribute to the pathogenic complexity of the inflammatory process [6]. In addition to inflammation, other mechanisms such as lipid retention [7], neovascularization [1,5,8] and tissue remodeling [9,10] support plaque growth. How different leukocyte populations contribute to or are affected by these additional mechanisms remains elusive.…”

Section: Introductionmentioning

confidence: 99%

Invariant natural killer T cells: Linking inflammation and neovascularization in human atherosclerosis

et al. 2010

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Atherosclerosis, a chronic inflammatory lipid storage disease of large arteries, is complicated by cardiovascular events usually precipitated by plaque rupture or erosion. Inflammation participates in lesion progression and plaque rupture. Identification of leukocyte populations involved in plaque destabilization is important for effective prevention of cardiovascular events. This study investigates CD1d-expressing cells and invariant NKT cells (iNKT) in human arterial tissue, their correlation with disease severity and symptoms, and potential mechanisms for their involvement in plaque formation and/ or destabilization. CD1d-expressing cells were present in advanced plaques in patients who suffered from cardiovascular events in the past and were most abundant in plaques with ectopic neovascularization. Confocal microscopy detected iNKT cells in plaques, and plaque-derived iNKT cell lines promptly produced proinflammatory cytokines when stimulated by CD1d-expressing APC-presenting a-galactosylceramide lipid antigen. Furthermore, iNKT cells were diminished in the circulating blood of patients with symptomatic atherosclerosis. Activated iNKT cell-derived culture supernatants showed angiogenic activity in a human microvascular endothelial cell line HMEC-1-spheroid model of in vitro angiogenesis and strongly activated human microvascular endothelial cell line HMEC-1 migration. This functional activity was ascribed to IL-8 released by iNKT cells upon lipid recognition. These findings introduce iNKT cells as novel cellular candidates promoting plaque neovascularization and destabilization in human atherosclerosis.

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Metalloproteinases in Development and Progression of Vascular Disease

Cited by 95 publications

References 80 publications

Relationship Between Multiple Plasma Biomarkers and Vulnerable Plaque Determined by Virtual Histology Intravascular Ultrasound

Relationship Between Multiple Plasma Biomarkers and Vulnerable Plaque Determined by Virtual Histology Intravascular Ultrasound

Association of MMP‐9 gene polymorphisms with nephrolithiasis patients

Invariant natural killer T cells: Linking inflammation and neovascularization in human atherosclerosis

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