Polymorphisms of the methylenetetrahydrofolate reductase, vascular endothelial growth factor, endothelial nitric oxide synthase, monocyte chemoattractant protein-1 and apolipoprotein E genes are not associated with carotid intima-media thickness

Alioğlu, Emin; Türk, Uğur Önsel; Çam, Sırrı; Abbasaliyev, Abbasali; Tengiz, İstemihan; Ercan, Ertuğrul

doi:10.1016/s0828-282x(09)70022-4

Cited by 10 publications

(4 citation statements)

References 42 publications

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“…There are very few data about the association between IMT and VEGF in patients with coronary artery disease. In a small study, the authors found no differences in VEGF levels among patients with stable coronary artery disease and increased (above 1 mm) or normal IMT (below 1 mm) [ 20 ]. In the present study, we explored whether plasma VEGF levels were related to endothelial function, but found no significant correlation between FMD and VEGF levels.…”

Section: Discussionmentioning

confidence: 99%

Stable phase post-MI patients have elevated VEGF levels correlated with inflammation markers, but not with atherosclerotic burden

Eržen

Šilar

Šabovič

2014

BMC Cardiovasc Disord

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BackgroundThe role of vascular endothelial growth factor (VEGF) in patients in the stable phase after myocardial infarction (MI) has not yet been explored. Therefore, we compared the values of VEGF in post-MI patients with those obtained in healthy controls. Furthermore, we investigated whether the values of VEGF correlate to either inflammation markers or the atherosclerotic burden.Methods41 male patients (on average 44 years old) in the stable phase after MI (on average 20.5 months after MI) were recruited, while 25 healthy age-matched males served as controls. Plasma levels of VEGF and several markers of inflammation were measured by standard procedures. The atherosclerotic burden was determined by the angiographic severity of coronary atherosclerosis, endothelial dysfunction (measured by ultrasound measurement of the flow mediated dilation of the brachial artery), the intima-media thickness of the common carotid artery and the ankle-brachial pressure index.ResultsVEGF values were significantly elevated in post-MI patients compared to the controls (53.8 ± 42.7 pg/ml vs. 36.3 ± 8.9 pg/ml, p = 0.014). The elevated VEGF values significantly correlated to the (increased) values of the inflammatory molecules interleukin 6 and 8 (r = 0.37, p = 0.017; and r = 0.45, p = 0.003; respectively). In contrast, no correlation was found between VEGF and the parameters of the atherosclerotic burden, although FMD and IMT were significantly impaired in patients.ConclusionsWe found that plasma levels of VEGF are increased in the stable phase after MI and correlate with inflammation cytokines, but not with the atherosclerotic burden. Thus, this suggests that increased levels of VEGF are a part of ongoing inflammatory activity. Since VEGF in these patients stimulates neovascularization of inflamed plaques and induces their destabilization, the VEGF level can have an important negative prognostic value. Clearly, further studies are needed to clarify the role of VEGF as a prognostic marker.

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Section: Discussionmentioning

confidence: 99%

Stable phase post-MI patients have elevated VEGF levels correlated with inflammation markers, but not with atherosclerotic burden

Eržen

Šilar

Šabovič

2014

BMC Cardiovasc Disord

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“…Genetic polymorphisms in the homologous region on human chromosome 17 have been studied for involvement in MS susceptibility, [29][30][31][32] as well as other autoimmune or chronic inflammatory diseases including RA, 60 myocardial infarction 66,67 and allergy. 68 A second cluster including chemokine genes (CCL5, CCL16, CCL14, CCL15, CCL23, CCL18, CCL3 and CCL4) located further upstream has also been studied in relation to MS, but in this study we have focused on the centromeric cluster, as this was identified in the rat linkage study.…”

Section: Discussionmentioning

confidence: 99%

Genetic variants of CC chemokine genes in experimental autoimmune encephalomyelitis, multiple sclerosis and rheumatoid arthritis

et al. 2009

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Multiple sclerosis (MS) is a complex disorder of the central nervous system, causing inflammation, demyelination and axonal damage. A limited number of genetic risk factors for MS have been identified, but the etiology of the disease remains largely unknown. For the identification of genes regulating neuroinflammation we used a rat model of MS, myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), and carried out a linkage analysis in an advanced intercross line (AIL). We thereby redefine the Eae18b locus to a 0.88 Mb region, including a cluster of chemokine genes. Further, we show differential expression of Ccl2, Ccl11 and Ccl11 during EAE in rat strains with opposite susceptibility to EAE, regulated by genotype in Eae18b. The human homologous genes were tested for association to MS in 3841 cases and 4046 controls from four Nordic countries. A haplotype in CCL2 and rs3136682 in CCL1 show a protective association to MS, whereas a haplotype in CCL13 is disease predisposing. In the HLA-DRB1*15 positive subgroup, we also identified an association to a risk haplotype in CCL2, suggesting an influence from the human leukocyte antigen (HLA) locus. We further identified association to rheumatoid arthritis in CCL2, CCL8 and CCL13, indicating common regulatory mechanisms for complex diseases.

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“…However, 28 studies were further excluded because they were found to have no direct relationship to the topic, after reading the full text of the articles. Furthermore, one case-only study (Alioglu et al, 2009) and two family-based studies (McGlinchey et al, 2004;Kim et al, 2007) were also excluded. Finally, 21 studies (Szalai et al, 2001;Simeoni et al, 2004;Cermakova et al, 2005;McDermott et al, 2005;Bjarnadottir et al, 2006;Iwai et al, 2006;Cam et al, 2008;Bucova et al, 2008;Jemaa et al, 2008;Bucova et al, 2009a;Bucova et al, 2009b;Zhang et al, 2009;Zhong et al, 2010;van Wijk et al, 2010;El Mahgoub et al, 2011;Lin et al, 2012;Wang & Zhang, 2012;Yang et al, 2012;Xu et al, 2013;Kaur et al, 2013;Nasibullin et al, 2014) with a total of 8,735 cases and 12,300 controls were included in this meta-analysis.…”

Section: Eligible Studies Included In the Meta-analysismentioning

confidence: 99%

Association of Monocyte Chemoattractant Protein‐1 (MCP‐1)‐2518A>G Polymorphism with Susceptibility to Coronary Artery Disease: A Meta‐Analysis

Bai

Wang

et al. 2015

Annals of Human Genetics

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SummaryWe attempted to systematically elucidate the association between monocyte chemoattractant protein-1 (MCP-1) -2518A>G polymorphism and risk of coronary artery disease (CAD). Eligible studies were identified through PubMed, EBSCO, and Web of Science Databases. The magnitude of MCP-1 polymorphism effect and its possible mode of action on CAD were estimated. The odds ratio (OR) with 95% confidence intervals (CI) were pooled in a specific genetic model to assess the association. A total of 21 studies were involved. There was significant gene effect on CAD risk in the overall population (likelihood ratio test: p < 0.0001). Patients with GG and AG genotypes had 1.435 (95% CI: 1.183-1.740) and 1.087 (95% CI: 1.008-1.172) times higher risk of CAD than those with AA genotype. These gene effects suggested a recessive model to be appropriate. The pooled OR was 1.362 (95% CI: 1.137-1.631; p uncorrected = 0.001, p FDR = 0.005) in the recessive model. In the ethnicity-stratified analysis, significant association was observed in the Caucasian population (OR = 1.492; 95% CI: 1.106-2.014; p uncorrected = 0.009, p FDR = 0.015), whereas no statistical significant association was detected in the Asian population (adjusted p = 0.124). The results suggested that MCP-1 -2518A>G polymorphism may be associated with susceptibility to CAD, especially in Caucasians.

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Polymorphisms of the methylenetetrahydrofolate reductase, vascular endothelial growth factor, endothelial nitric oxide synthase, monocyte chemoattractant protein-1 and apolipoprotein E genes are not associated with carotid intima-media thickness

Cited by 10 publications

References 42 publications

Stable phase post-MI patients have elevated VEGF levels correlated with inflammation markers, but not with atherosclerotic burden

Stable phase post-MI patients have elevated VEGF levels correlated with inflammation markers, but not with atherosclerotic burden

Genetic variants of CC chemokine genes in experimental autoimmune encephalomyelitis, multiple sclerosis and rheumatoid arthritis

Association of Monocyte Chemoattractant Protein‐1 (MCP‐1)‐2518A>G Polymorphism with Susceptibility to Coronary Artery Disease: A Meta‐Analysis

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