Functional polymorphisms in the LTF gene and risk of coronary artery stenosis

Videm, Vibeke; Dahl, Hildegunn; Wålberg, Lise Eid; Wiseth, Rune

doi:10.1016/j.humimm.2012.02.014

Cited by 20 publications

(23 citation statements)

References 28 publications

(35 reference statements)

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“…Since these authors did not identify alleles A and G (and described them only as alleles 1 and 2), it is not possible to say which variant (A or G) was a risk factor for or protective against dental caries in their study. In contrast to European subjects, in Asian, African and American populations, G is the dominant allele, with a frequency of 0.7-0.9 [Videm et al, 2012], and this allele was also previously associated with an increased risk of periodontitis [Velliyagounder et al, 2003;Wu et al, 2009]. The LTF polymorphism analyzed in this study was the same as the variant analyzed by Azevedo et al [2010], but there were some differences in methodology and sample size.…”

Section: Discussionmentioning

confidence: 60%

“…function. In turn, this may lead to reduced defense against infections with stronger stimuli for granulocyte activation and degranulation, which results in higher LTF release [Videm et al, 2012]. In addition, it was suggested that the oral microbiota of subjects harboring 1 or 2 Lyscontaining alleles contains lower levels of Streptococcus mutans due to the increased antibacterial activity of this variant against Gram-positive bacteria [Velliyagounder et al, 2003].…”

Section: Discussionmentioning

confidence: 99%

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Lack of Association between Lactotransferrin Polymorphism and Dental Caries

et al. 2013

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Objective: Dental caries is a complex, multifactorial disease and one of the most common illnesses worldwide. Its etiology is related to microbial, dietary and host factors. Recent evidence suggests a role of lactotransferrin (LTF) in caries. The purpose of this study was to determine the association between LTF gene polymorphism and dental caries. Methods: In this case-control study, 637 unrelated children, aged 11-13 years, were enrolled. The subjects were divided into two groups, i.e. caries-free (decayed/missing/filled teeth = 0) and caries-affected children (decayed/missing/filled teeth ≥ 1). The LTF rs1126478 (140A/G in exon 2, Lys/Arg) genotypes were determined by PCR with restriction analysis using the EarI enzyme. Results: Of 637 children, 155 (24.3%) were caries free. There were no statistically significant differences between caries levels and allele or genotype distributions in the total cohort. When the caries-affected group (n = 482) was stratified into low (decayed/missing/filled teeth = 1), moderate (2 ≤ decayed/missing/filled teeth ≤ 3) and high (decayed/missing/filled teeth ≥ 4) caries experience, allele and genotype frequencies were similar among all subgroups. Conclusions: The LTF 140A/G (exon 2, Lys/Arg) polymorphism was not associated with the susceptibility to or severity of dental caries in the Czech population.

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Lack of Association between Lactotransferrin Polymorphism and Dental Caries

et al. 2013

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“…Later, data on other genetic markers in this population have also been published [14], [15]. Briefly, the patients with available samples for the present pilot study (n = 234 due to 2 lost samples) consisted of 131 patients with significant (>50%) artery stenosis in at least one main coronary artery branch and 103 patients without significant coronary artery stenosis, as demonstrated by quantitative coronary angiography.…”

Section: Methodsmentioning

confidence: 99%

Mannose-Binding Lectin Deficiency Is Associated with Myocardial Infarction: The HUNT2 Study in Norway

et al. 2012

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ObjectivesMannose-binding lectin (MBL) and ficolins activate the complement cascade, which is involved in atherogenesis. Based on a pilot study, we hypothesized that functional polymorphisms in the MBL gene (MBL2) leading to dysfunctional protein are related to development of myocardial infarction (MI). The aim of the present study was to study polymorphisms in MBL2 and ficolin genes in relation to the risk of MI.Methods and ResultsUsing the population-based HUNT Study in Norway, 57133 persons were followed up for a first-time MI from 1995–1997 until the end of 2008. The 370 youngest MI patients were matched by age (range 29–62 years) and gender to 370 controls. A younger population was selected because disease in this group might be less dependent on non-genetic risk factors. The study size was based on power calculation. Polymorphisms in MBL2 and in the genes of ficolin-1, ficolin-2 and ficolin-3 were genotyped by pyrosequencing and related to the risk of MI, estimated as odds ratios (OR). Functional haplotypes were analyzed and stringent alpha levels of significance were set by permutation testing. Variant MBL2 haplotypes causing MBL deficiency were associated with a two-fold higher risk of MI (OR 2.04, 95%CI 1.29–3.24). Adjustments for conventional cardiovascular risk factors did not substantially influence the association. The ficolins were not associated with MI risk.ConclusionIn a young to middle aged and relatively healthy Caucasian population, MBL2 variants related to functional MBL deficiency were associated with a doubling of the risk for MI, independent of conventional risk factors. This supports that MBL deficiency may lead to increased atherosclerosis or development of vulnerable plaques.

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“…Genotyping for the lactoferrin (LTF) gene was carried out by Sanger sequencing. 10 Twenty-seven other SNPs were analysed by Centre for Integrative Genetics (CIGENE, Norwegian University of Life Sciences, Ås, Norway) using Sequenom MassArray technology (Sequenom, San Diego, CA, USA).…”

Section: Snp Selection and Genotypingmentioning

confidence: 99%