A haplotype constituted of four MMP-2 promoter polymorphisms (−1575G/A, −1306C/T, −790T/G and −735C/T) is associated with coronary triple-vessel disease

Vašků, Anna; Goldbergová, Monika Pávková; Hollá, Lýdie Izakovičová; Šišková, Lenka; Groch, Ladislav; Beránek, Michal; Tschöplová, Svatava; Znojil, Vladimı́r; Vácha, Jiří

doi:10.1016/j.matbio.2003.10.004

Cited by 60 publications

(22 citation statements)

References 22 publications

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“…In the Xu et al [104] cohort of 126 CRC patients and 126 control patients, two other polymorphisms of MMP2 (790 T/G, 955 A/C) were not associated with cancer susceptibility or infiltration depth, while GG genotype carriers of the MMP2 1575 G/A polymorphism had an increased risk of developing CRC and more frequent serosa or adventitia invasion compared to the other geno types, similar to that with the 1306 CC genotype [102] . The similarity in these observations are probably because the MMP2 1575 G/A, 1306 C/T, 790 G/T and 735 C/T polymorphisms have been found to be in almost complete pairwise linkage (dis)equilibrium [28] . The most frequently studied MMP9 polymorphism is the C to T substitution at position 1562 of the pro moter region, which increases transcriptional activity.…”

Section: Colorectal Cancermentioning

confidence: 62%

“…Table 3 gives an overview of the studies discussed in this paragraph. [18] MMP-2 -1306 C/T C to T substitution disrupts Sp-1 binding site Decreased in T-allele Price et al [22] MMP-2 -735 C/T C to T substitution influences Sp-1 binding site Decreased in T-allele Yu et al [15] MMP-2 -790 T/G Three transcription factors 1 bind to T (but not G) allele sequence Decreased in G allele 2 Vasku et al [28] MMP-2 -955 A/C Unknown Effect unclear Price et al [22] MMP-2 -1575 G/A G to T substitution decreases estrogen receptor α binding Decreased in A allele Harendza et al [27] MMP-3 -1171 5A/6A…”

Section: Gastric Cancermentioning

confidence: 99%

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Single-nucleotide polymorphisms of matrix metalloproteinases and their inhibitors in gastrointestinal cancer

Langers

Verspaget²,

Hommes³

et al. 2011

WJGO

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Matrix metalloproteinases (MMPs) are implicated in cancer development and progression and are associated with prognosis. Single-nucleotide polymorphisms (SNPs) of MMPs, most frequently located in the promoter region of the genes, have been shown to influence cancer susceptibility and/or progression. SNPs of MMP-1, -2, -3, -7, -8, -9, -12, -13 and -21 and of the tissue inhibitor of metalloproteinases (TIMPs) TIMP-1 and TIMP-2 have been studied in digestive tract tumors. The contribution of these polymorphisms to the cancer risk and prognosis of gastrointestinal tumors are reviewed in this paper.

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Section: Colorectal Cancermentioning

confidence: 62%

Section: Gastric Cancermentioning

confidence: 99%

Single-nucleotide polymorphisms of matrix metalloproteinases and their inhibitors in gastrointestinal cancer

Langers

Verspaget²,

Hommes³

et al. 2011

WJGO

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“…Clinical studies have now identified variant forms contained within the DNA sequences of MMP genes, or polymorphisms, for several of the MMP subtypes (25,30,65,163,240,241,258,273,277,304,329,377,440,466,514,539). The polymorphisms that have been identified thus far often affect the promoter region of the MMP gene, and thereby influence critical steps in the binding of transcription factors or the overall efficiency of transcription.…”

Section: Gene Polymorphism Observationsmentioning

confidence: 99%

“…MMP-2 polymorphisms comprising a single substitution within the promoter region (Ϫ1306C/T or Ϫ790T/G) have been examined in clinical studies (277,466). While these variants in the MMP-2 promoter may cause increased transcriptional activity, the relationship to adverse LV remodeling or cardiovascular events remains to be established.…”

Section: Gene Polymorphism Observationsmentioning

confidence: 99%

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Spinale¹

2007

Physiological Reviews

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1,023

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It is now becoming apparent that dynamic changes occur within the interstitium that directly contribute to adverse myocardial remodeling following myocardial infarction (MI), with hypertensive heart disease and with intrinsic myocardial disease such as cardiomyopathy. Furthermore, a family of matrix proteases, the matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs), has been recognized to play an important role in matrix remodeling in these cardiac disease states. The purpose of this review is fivefold: 1) to examine and redefine the myocardial matrix as a critical and dynamic entity with respect to the remodeling process encountered with MI, hypertension, or cardiomyopathic disease; 2) present the remarkable progress that has been made with respect to MMP/TIMP biology and how it relates to myocardial matrix remodeling; 3) to evaluate critical translational/clinical studies that have provided a cause-effect relationship between alterations in MMP/TIMP regulation and myocardial matrix remodeling; 4) to provide a critical review and analysis of current diagnostic, prognostic, and pharmacological approaches that utilized our basic understanding of MMP/TIMPs in the context of cardiac disease; and 5) most importantly, to dispel the historical belief that the myocardial matrix is a passive structure and supplant this belief that the regulation of matrix protease pathways such as the MMPs and TIMPs will likely yield a new avenue of diagnostic and therapeutic strategies for myocardial remodeling and the progression to heart failure.

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“…However, studies identifying which of these polymorphisms, if any, are associated with specific cardiovascular diseases have been less successful. Many are based on small sample sizes, [11][12][13] require replication, 14,15 or conflict with results of other studies. 16,17 In addition, many of the studies are based on late-stage cardiovascular diseases, making meta-analysis impossible because of differing underlying pathology and end points used.…”

mentioning

confidence: 99%

Polymorphisms in MMP Family and TIMP Genes and Carotid Artery Intima-Media Thickness

Armstrong

Abilleira

Sitzer

et al. 2007

Stroke

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Background and Purpose-Genetic variation in a number of MMP and TIMP genes have been implicated as risk factors for atherosclerosis, although such studies have been generally small and produced conflicting results. We have therefore sought to address this issue in a large, well-phenotyped community population to assess the effect of a number of polymorphisms in both MMP and TIMP genes on carotid artery intima-media thickness (IMT). Methods-In a community population (nϭ1000), IMT was determined using ultrasound in the common carotid artery, carotid bulb, and bifurcation. Eight polymorphisms in 6 MMP genes were genotyped (MMP1 A-519G, MMP2 C-1306T, MMP2 C-735T, MMP3 -1171 5A/6A, MMP9 R279Q, TIMP2 G853A, TIMP3 A-915G, and T-1296C) and assessed for their effect on carotid IMT alone and by interaction with common cardiovascular risk factors. Results-An association was found between MMP9 R279Q and internal carotid artery bulb IMT (Pϭ0.002), but there was no linear trend between allele number and IMT and no association with common carotid artery or bulb IMT. In addition, 3 interactions were found between polymorphisms and hypertension (MMP1 A-519G, MMP3 5A/6A, TIMP3 T-1296C), the latter 2 of which showed a significant trend test for linearity with increasing copy number and increased internal carotid artery bulb IMT. All remained significant after correction for multiple testing. Conclusions-Our findings provide little support for genetic variants of MMP as direct risk factors for IMT. However, the interaction findings between MMP variants and hypertension suggest that hypertensive carriers of these alleles may be at greater risk for increased IMT and future cardiovascular disease. These findings need replication in hypertensive populations to assess their effects more fully.

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A haplotype constituted of four MMP-2 promoter polymorphisms (−1575G/A, −1306C/T, −790T/G and −735C/T) is associated with coronary triple-vessel disease

Cited by 60 publications

References 22 publications

Single-nucleotide polymorphisms of matrix metalloproteinases and their inhibitors in gastrointestinal cancer

Single-nucleotide polymorphisms of matrix metalloproteinases and their inhibitors in gastrointestinal cancer

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Polymorphisms in MMP Family and TIMP Genes and Carotid Artery Intima-Media Thickness

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