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The relation of genetic and environmental factors to systemic inflammatory biomarker concentrations

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The relation of genetic and environmental factors to systemic inflammatory biomarker concentrations. / Schnabel, Renate B; Lunetta, Kathryn L; Larson, Martin G; Dupuis, Josée; Lipinska, Izabella; Rong, Jian; Chen, Ming-Huei; Zhao, Zhenming; Yamamoto, Jennifer F; Meigs, James B; Nicaud, Viviane; Perret, Claire; Zeller, Tanja; Blankenberg, Stefan; Tiret, Laurence; Keaney, John F; Vasan, Ramachandran S; Benjamin, Emelia J.

In: CIRC-CARDIOVASC GENE, Vol. 2, No. 3, 06.2009, p. 229-37.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Schnabel, RB, Lunetta, KL, Larson, MG, Dupuis, J, Lipinska, I, Rong, J, Chen, M-H, Zhao, Z, Yamamoto, JF, Meigs, JB, Nicaud, V, Perret, C, Zeller, T, Blankenberg, S, Tiret, L, Keaney, JF, Vasan, RS & Benjamin, EJ 2009, 'The relation of genetic and environmental factors to systemic inflammatory biomarker concentrations', CIRC-CARDIOVASC GENE, vol. 2, no. 3, pp. 229-37. https://doi.org/10.1161/CIRCGENETICS.108.804245

APA

Schnabel, R. B., Lunetta, K. L., Larson, M. G., Dupuis, J., Lipinska, I., Rong, J., Chen, M-H., Zhao, Z., Yamamoto, J. F., Meigs, J. B., Nicaud, V., Perret, C., Zeller, T., Blankenberg, S., Tiret, L., Keaney, J. F., Vasan, R. S., & Benjamin, E. J. (2009). The relation of genetic and environmental factors to systemic inflammatory biomarker concentrations. CIRC-CARDIOVASC GENE, 2(3), 229-37. https://doi.org/10.1161/CIRCGENETICS.108.804245

Vancouver

Schnabel RB, Lunetta KL, Larson MG, Dupuis J, Lipinska I, Rong J et al. The relation of genetic and environmental factors to systemic inflammatory biomarker concentrations. CIRC-CARDIOVASC GENE. 2009 Jun;2(3):229-37. https://doi.org/10.1161/CIRCGENETICS.108.804245

Bibtex

@article{cee5817ccdaa41f5a7d63172d42695d2,
title = "The relation of genetic and environmental factors to systemic inflammatory biomarker concentrations",
abstract = "BACKGROUND: Environmental and genetic correlates of inflammatory marker variability are incompletely understood. In the family-based Framingham Heart Study, we investigated heritability and candidate gene associations of systemic inflammatory biomarkers.METHODS AND RESULTS: In offspring participants (n=3710), we examined 11 inflammatory biomarkers (CD40 ligand, C-reactive protein, intercellular adhesion molecule-1, interleukin-6, urinary isoprostanes, monocyte chemoattractant protein-1, myeloperoxidase, P-selectin, tumor necrosis factor-alpha, tumor necrosis factor receptor II, fibrinogen). Heritability and bivariate genetic and environmental correlations were assessed by Sequential Oligogenic Linkage Analysis routines in 1012 family members. We examined 1943 tagging single-nucleotide polymorphisms in 233 inflammatory pathway genes with >or=5 minor allele carriers using a general genetic linear model. Clinical correlates explained 2.4% (CD40 ligand) to 28.5% (C-reactive protein) of the variability in inflammatory biomarkers. Estimated heritability ranged from 10.9% (isoprostanes) to 44.8% (P-selectin). Most correlations between biomarkers were weak although statistically significant. A total of 45 single-nucleotide polymorphism-biomarker associations met the q-value threshold of 0.25. Novel top single-nucleotide polymorphisms were observed in ICAM1 gene in relation to intercellular adhesion molecule-1 concentrations (rs1799969, P=1.32 x 10(-8)) and MPO in relation to myeloperoxidase (rs28730837, P=1.9 x 10(-5)). Lowest P values for trans-acting single-nucleotide polymorphisms were observed for APCS with monocyte chemoattractant protein-1 concentrations (rs1374486, P=1.01 x 10(-7)) and confirmed for IL6R with interleukin-6 concentrations (rs8192284, P=3.36 x 10(-5)). Novel potential candidates (APCS, MPO) need to be replicated.CONCLUSIONS: Our community-based data support the relevance of clinical and genetic factors for explaining variation in inflammatory biomarker traits.",
keywords = "Alleles, Biomarkers/analysis, Cohort Studies, Community-Based Participatory Research, Gene Frequency, Humans, Inflammation/genetics, Inflammation Mediators/analysis, Multivariate Analysis, Phenotype, Polymorphism, Single Nucleotide, Risk Factors",
author = "Schnabel, {Renate B} and Lunetta, {Kathryn L} and Larson, {Martin G} and Jos{\'e}e Dupuis and Izabella Lipinska and Jian Rong and Ming-Huei Chen and Zhenming Zhao and Yamamoto, {Jennifer F} and Meigs, {James B} and Viviane Nicaud and Claire Perret and Tanja Zeller and Stefan Blankenberg and Laurence Tiret and Keaney, {John F} and Vasan, {Ramachandran S} and Benjamin, {Emelia J}",
year = "2009",
month = jun,
doi = "10.1161/CIRCGENETICS.108.804245",
language = "English",
volume = "2",
pages = "229--37",
journal = "CIRC-CARDIOVASC GENE",
issn = "1942-325X",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

RIS

TY - JOUR

T1 - The relation of genetic and environmental factors to systemic inflammatory biomarker concentrations

AU - Schnabel, Renate B

AU - Lunetta, Kathryn L

AU - Larson, Martin G

AU - Dupuis, Josée

AU - Lipinska, Izabella

AU - Rong, Jian

AU - Chen, Ming-Huei

AU - Zhao, Zhenming

AU - Yamamoto, Jennifer F

AU - Meigs, James B

AU - Nicaud, Viviane

AU - Perret, Claire

AU - Zeller, Tanja

AU - Blankenberg, Stefan

AU - Tiret, Laurence

AU - Keaney, John F

AU - Vasan, Ramachandran S

AU - Benjamin, Emelia J

PY - 2009/6

Y1 - 2009/6

N2 - BACKGROUND: Environmental and genetic correlates of inflammatory marker variability are incompletely understood. In the family-based Framingham Heart Study, we investigated heritability and candidate gene associations of systemic inflammatory biomarkers.METHODS AND RESULTS: In offspring participants (n=3710), we examined 11 inflammatory biomarkers (CD40 ligand, C-reactive protein, intercellular adhesion molecule-1, interleukin-6, urinary isoprostanes, monocyte chemoattractant protein-1, myeloperoxidase, P-selectin, tumor necrosis factor-alpha, tumor necrosis factor receptor II, fibrinogen). Heritability and bivariate genetic and environmental correlations were assessed by Sequential Oligogenic Linkage Analysis routines in 1012 family members. We examined 1943 tagging single-nucleotide polymorphisms in 233 inflammatory pathway genes with >or=5 minor allele carriers using a general genetic linear model. Clinical correlates explained 2.4% (CD40 ligand) to 28.5% (C-reactive protein) of the variability in inflammatory biomarkers. Estimated heritability ranged from 10.9% (isoprostanes) to 44.8% (P-selectin). Most correlations between biomarkers were weak although statistically significant. A total of 45 single-nucleotide polymorphism-biomarker associations met the q-value threshold of 0.25. Novel top single-nucleotide polymorphisms were observed in ICAM1 gene in relation to intercellular adhesion molecule-1 concentrations (rs1799969, P=1.32 x 10(-8)) and MPO in relation to myeloperoxidase (rs28730837, P=1.9 x 10(-5)). Lowest P values for trans-acting single-nucleotide polymorphisms were observed for APCS with monocyte chemoattractant protein-1 concentrations (rs1374486, P=1.01 x 10(-7)) and confirmed for IL6R with interleukin-6 concentrations (rs8192284, P=3.36 x 10(-5)). Novel potential candidates (APCS, MPO) need to be replicated.CONCLUSIONS: Our community-based data support the relevance of clinical and genetic factors for explaining variation in inflammatory biomarker traits.

AB - BACKGROUND: Environmental and genetic correlates of inflammatory marker variability are incompletely understood. In the family-based Framingham Heart Study, we investigated heritability and candidate gene associations of systemic inflammatory biomarkers.METHODS AND RESULTS: In offspring participants (n=3710), we examined 11 inflammatory biomarkers (CD40 ligand, C-reactive protein, intercellular adhesion molecule-1, interleukin-6, urinary isoprostanes, monocyte chemoattractant protein-1, myeloperoxidase, P-selectin, tumor necrosis factor-alpha, tumor necrosis factor receptor II, fibrinogen). Heritability and bivariate genetic and environmental correlations were assessed by Sequential Oligogenic Linkage Analysis routines in 1012 family members. We examined 1943 tagging single-nucleotide polymorphisms in 233 inflammatory pathway genes with >or=5 minor allele carriers using a general genetic linear model. Clinical correlates explained 2.4% (CD40 ligand) to 28.5% (C-reactive protein) of the variability in inflammatory biomarkers. Estimated heritability ranged from 10.9% (isoprostanes) to 44.8% (P-selectin). Most correlations between biomarkers were weak although statistically significant. A total of 45 single-nucleotide polymorphism-biomarker associations met the q-value threshold of 0.25. Novel top single-nucleotide polymorphisms were observed in ICAM1 gene in relation to intercellular adhesion molecule-1 concentrations (rs1799969, P=1.32 x 10(-8)) and MPO in relation to myeloperoxidase (rs28730837, P=1.9 x 10(-5)). Lowest P values for trans-acting single-nucleotide polymorphisms were observed for APCS with monocyte chemoattractant protein-1 concentrations (rs1374486, P=1.01 x 10(-7)) and confirmed for IL6R with interleukin-6 concentrations (rs8192284, P=3.36 x 10(-5)). Novel potential candidates (APCS, MPO) need to be replicated.CONCLUSIONS: Our community-based data support the relevance of clinical and genetic factors for explaining variation in inflammatory biomarker traits.

KW - Alleles

KW - Biomarkers/analysis

KW - Cohort Studies

KW - Community-Based Participatory Research

KW - Gene Frequency

KW - Humans

KW - Inflammation/genetics

KW - Inflammation Mediators/analysis

KW - Multivariate Analysis

KW - Phenotype

KW - Polymorphism, Single Nucleotide

KW - Risk Factors

U2 - 10.1161/CIRCGENETICS.108.804245

DO - 10.1161/CIRCGENETICS.108.804245

M3 - SCORING: Journal article

C2 - 20031590

VL - 2

SP - 229

EP - 237

JO - CIRC-CARDIOVASC GENE

JF - CIRC-CARDIOVASC GENE

SN - 1942-325X

IS - 3

ER -