Inflammation-sensitive proteins and risk of atrial fibrillation: a population-based cohort study

Eryd, Samuel Adamsson; Smith, J. G.; Melander, Olle; Hedblad, Bo; Engström, Gunnar

doi:10.1007/s10654-011-9565-6

Cited by 36 publications

(17 citation statements)

References 39 publications

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“…The participation rate was 71%. As a part of the programme, plasma levels of ceruloplasmin were determined for a random sample of 6455 men . Of these men, 3907 were later re‐examined in follow‐up studies including DNA sampling ; the mean age at baseline was 46.3 ± 3.6 years.…”

Section: Methodsmentioning

confidence: 99%

Ceruloplasmin and atrial fibrillation: evidence of causality from a population‐based Mendelian randomization study

et al. 2013

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Objectives. Inflammatory diseases and inflammatory markers secreted by the liver, including C-reactive protein (CRP) and ceruloplasmin, have been associated with incident atrial fibrillation (AF). Genetic studies have not supported a causal relationship between CRP and AF, but the relationship between ceruloplasmin and AF has not been studied. The purpose of this Mendelian randomization study was to explore whether genetic polymorphisms in the gene encoding ceruloplasmin are associated with elevated ceruloplasmin levels, and whether such genetic polymorphisms are also associated with the incidence of AF.Design. Genetic polymorphisms in the ceruloplasmin gene (CP) were genotyped in a population-based cohort study of men from southern Sweden (Malm€ o Preventive Project; n = 3900). Genetic polymorphisms associated with plasma ceruloplasmin concentration were also investigated for association with incident AF (n = 520) during a mean follow-up of 29 years in the same cohort. Findings were replicated in an independent case-control sample (The Malm€ o AF cohort; n = 2247 cases, 2208 controls).Results. A single nucleotide polymorphism (rs1170 8215, minor allele frequency 0.12) located in the CP gene promoter was strongly associated with increased levels of plasma ceruloplasmin (P = 9 9 10 À10) and with AF in both the discovery cohort [hazard ratio 1.24 per risk allele, 95% confidence interval (CI) 1.06-1.44, P = 0.006] and the replication cohort (odds ratio 1.13, 95% CI 1.02-1.26, P = 0.02).Conclusions. Our findings indicate a causal role of ceruloplasmin in AF pathophysiology and suggest that ceruloplasmin might be a mediator in a specific inflammatory pathway that causally links inflammatory diseases and incidence of AF.

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Section: Methodsmentioning

confidence: 99%

Ceruloplasmin and atrial fibrillation: evidence of causality from a population‐based Mendelian randomization study

et al. 2013

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“…The inflammatory process is considered to be one of the mechanisms for the genesis of cardiac arrhythmias [20,21]. In this study, adipocytokines derived from both epicardial and limb fat tissues significantly decreased I K in H9c2 cells, and the degree of suppression of I K was significantly more prominent with adipocytokines from pericardial than with those from limb fat tissues.…”

Section: Discussionmentioning

confidence: 54%

Differential Effects of Central and Peripheral Fat Tissues on the Delayed Rectifier K<sup>+</sup> Outward Currents in Cardiac Myocytes

Lee¹,

Tang

Tsai

et al. 2013

Cardiology

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Objectives: The amount of fat tissue is associated with an increasing incidence of cardiac arrhythmias. The purpose of this study was to investigate effects of adipocytokines from different body fat on delayed rectifier K⁺ outward currents (I_K). Methods: H9c2 cells were treated with adipocytokine-free medium (the Adipo-free group) and with adipocytokines from epicardial (central fat group) and limb (peripheral fat group) rat fat tissues. I_K, as well as expressions of Kv2.1 and Kv2.1 mRNA in H9c2 cells, were measured and compared between different groups. Results: I_K measured in H9c2 cells immediately after treatment with adipocytokines were not significantly different from those treated with adipocytokine-free medium. After H9c2 cells were treated with adipocytokines for 18 h, I_K were significantly decreased in the peripheral and central fat groups in comparison with the Adipo-free group. Compared with the peripheral fat group, I_K were more significantly decreased in the central fat group. Expressions of Kv2.1 and Kv2.1 mRNA in H9c2 cells were not significantly different among the three groups. Conclusions: Adipocytokines significantly decreased I_K in H9c2 cells, and I_K was more prominently decreased by adipocytokines from epicardial fat than from limb fat tissues. The decrease in I_K by adipocytokines may partially contribute to the mechanisms of arrhythmogenesis by fat tissues.

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“…Known markers of inflammation, such as haptoglobin and SAA, were among the proteins identified. Studies from the Malmö Preventive Study, Sweden, have shown that elevated plasma levels of haptoglobin are a risk factor for MI [19]. Recently, Devaux's group identified haptoglobin as a potential biomarker of prognosis of heart failure in patients with acute MI [20].…”

Section: Discussionmentioning

confidence: 99%

Plasma Fractionation Enriches Post-Myocardial Infarction Samples Prior to Proteomics Analysis

Brás

DeLeon

et al. 2012

International Journal of Proteomics

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Following myocardial infarction (MI), matrix metalloproteinase-9 (MMP-9) levels increase, and MMP-9 deletion improves post-MI remodeling of the left ventricle (LV). We provide here a technical report on plasma-analysis from wild type (WT) and MMP-9 null mice using fractionation and mass-spectrometry-based proteomics. MI was induced by coronary artery ligation in male WT and MMP-9 null mice (4–8 months old; n = 3/genotype). Plasma was collected on days 0 (pre-) and 1 post-MI. Plasma proteins were fractionated and proteins in the lowest (fraction 1) and highest (fraction 12) molecular weight fractions were separated by 1-D SDS-PAGE, digested in-gel with trypsin and analyzed by HPLC-ESI-MS/MS on an Orbitrap Velos. We tried five different fractionation protocols, before reaching an optimized protocol that allowed us to identify over 100 proteins. Serum amyloid A substantially increased post-MI in both genotypes, while alpha-2 macroglobulin increased only in the null samples. In fraction 12, extracellular matrix proteins were observed only post-MI. Interestingly, fibronectin-1, a substrate of MMP-9, was identified at both day 0 and day 1 post-MI in the MMP-9 null mice but was only identified post-MI in the WT mice. In conclusion, plasma fractionation offers an improved depletion-free method to evaluate plasma changes following MI.

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Inflammation-sensitive proteins and risk of atrial fibrillation: a population-based cohort study

Cited by 36 publications

References 39 publications

Ceruloplasmin and atrial fibrillation: evidence of causality from a population‐based Mendelian randomization study

Ceruloplasmin and atrial fibrillation: evidence of causality from a population‐based Mendelian randomization study

Differential Effects of Central and Peripheral Fat Tissues on the Delayed Rectifier K<sup>+</sup> Outward Currents in Cardiac Myocytes

Plasma Fractionation Enriches Post-Myocardial Infarction Samples Prior to Proteomics Analysis

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