Genome-Wide Association Analysis of Soluble ICAM-1 Concentration Reveals Novel Associations at the NFKBIK, PNPLA3, RELA, and SH2B3 Loci
Soluble ICAM-1 (sICAM-1) is an endothelium-derived inflammatory marker that has been associated with diverse conditions such as myocardial infarction, diabetes, stroke, and malaria. Despite evidence for a heritable component to sICAM-1 levels, few genetic loci have been identified so far. To compreh...
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| Vydáno v: | PLoS genetics Ročník 7; číslo 4; s. e1001374 |
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| Hlavní autoři: | , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
Public Library of Science
01.04.2011
Public Library of Science (PLoS) |
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| ISSN: | 1553-7404, 1553-7390, 1553-7404 |
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| Abstract | Soluble ICAM-1 (sICAM-1) is an endothelium-derived inflammatory marker that has been associated with diverse conditions such as myocardial infarction, diabetes, stroke, and malaria. Despite evidence for a heritable component to sICAM-1 levels, few genetic loci have been identified so far. To comprehensively address this issue, we performed a genome-wide association analysis of sICAM-1 concentration in 22,435 apparently healthy women from the Women's Genome Health Study. While our results confirm the previously reported associations at the ABO and ICAM1 loci, four novel associations were identified in the vicinity of NFKBIK (rs3136642, P = 5.4 × 10(-9)), PNPLA3 (rs738409, P = 5.8 × 10(-9)), RELA (rs1049728, P = 2.7 × 10(-16)), and SH2B3 (rs3184504, P = 2.9 × 10(-17)). Two loci, NFKBIB and RELA, are involved in NFKB signaling pathway; PNPLA3 is known for its association with fatty liver disease; and SH3B2 has been associated with a multitude of traits and disease including myocardial infarction. These associations provide insights into the genetic regulation of sICAM-1 levels and implicate these loci in the regulation of endothelial function. |
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| AbstractList | Soluble ICAM-1 (sICAM-1) is an endothelium-derived inflammatory marker that has been associated with diverse conditions such as myocardial infarction, diabetes, stroke, and malaria. Despite evidence for a heritable component to sICAM-1 levels, few genetic loci have been identified so far. To comprehensively address this issue, we performed a genome-wide association analysis of sICAM-1 concentration in 22,435 apparently healthy women from the Women's Genome Health Study. While our results confirm the previously reported associations at the ABO and ICAM1 loci, four novel associations were identified in the vicinity of NFKBIK (rs3136642, P = 5.4 × 10(-9)), PNPLA3 (rs738409, P = 5.8 × 10(-9)), RELA (rs1049728, P = 2.7 × 10(-16)), and SH2B3 (rs3184504, P = 2.9 × 10(-17)). Two loci, NFKBIB and RELA, are involved in NFKB signaling pathway; PNPLA3 is known for its association with fatty liver disease; and SH3B2 has been associated with a multitude of traits and disease including myocardial infarction. These associations provide insights into the genetic regulation of sICAM-1 levels and implicate these loci in the regulation of endothelial function. Soluble ICAM-1 (sICAM-1) is an endothelium-derived inflammatory marker that has been associated with diverse conditions such as myocardial infarction, diabetes, stroke, and malaria. Despite evidence for a heritable component to sICAM-1 levels, few genetic loci have been identified so far. To comprehensively address this issue, we performed a genome-wide association analysis of sICAM-1 concentration in 22,435 apparently healthy women from the Women's Genome Health Study. While our results confirm the previously reported associations at the ABO and ICAM1 loci, four novel associations were identified in the vicinity of NFKBIK (rs3136642, P = 5.4×10−9), PNPLA3 (rs738409, P = 5.8×10−9), RELA (rs1049728, P = 2.7×10−16), and SH2B3 (rs3184504, P = 2.9×10−17). Two loci, NFKBIB and RELA, are involved in NFKB signaling pathway; PNPLA3 is known for its association with fatty liver disease; and SH3B2 has been associated with a multitude of traits and disease including myocardial infarction. These associations provide insights into the genetic regulation of sICAM-1 levels and implicate these loci in the regulation of endothelial function. Soluble Intercellular Adhesion Molecule 1 (sICAM-1) is an inflammatory marker that has been associated with several common diseases such as diabetes, heart disease, stroke, and malaria. While it is known that blood concentrations of sICAM-1 are at least partially genetically determined, our current knowledge of which genes mediate this effect is limited. Taking advantage of technologies allowing us to interrogate genetic variation on a whole-genome basis, we found that variation in the NFKBIK, PNPLA3, RELA, and SH2B3 genes are important determinant of sICAM-1 blood concentrations. The NFKBIB and RELA genes are involved in regulation of inflammation. These observations are significant because this is the first report of genetic association within these extensively studied inflammation genes. The PNPLA3 gene has previously been associated with liver disease, and the SH2B3 gene has been associated with a multitude of traits including cardiovascular disease. Extension of these associations to sICAM-1 adds to the intriguing diversity of effects of these genes. Soluble ICAM-1 (sICAM-1) is an endothelium-derived inflammatory marker that has been associated with diverse conditions such as myocardial infarction, diabetes, stroke, and malaria. Despite evidence for a heritable component to sICAM-1 levels, few genetic loci have been identified so far. To comprehensively address this issue, we performed a genome-wide association analysis of sICAM-1 concentration in 22,435 apparently healthy women from the Women's Genome Health Study. While our results confirm the previously reported associations at the ABO and ICAM1 loci, four novel associations were identified in the vicinity of NFKBIK (rs3136642, P = 5.4 x [10.sup.-9]), PNPLA3 (rs738409, P = 5.8 x [10.sup.-9]), RELA (rs1049728, P = 2.7 x [10.sup.-16]), and SH2B3 (rs3184504, P = 2.9 x [10.sup.-17]). Two loci, NFKBIB and RELA, are involved in NFKB signaling pathway; PNPLA3 is known for its association with fatty liver disease; and SH3B2 has been associated with a multitude of traits and disease including myocardial infarction. These associations provide insights into the genetic regulation of sICAM-1 levels and implicate these loci in the regulation of endothelial function. Soluble ICAM-1 (sICAM-1) is an endothelium-derived inflammatory marker that has been associated with diverse conditions such as myocardial infarction, diabetes, stroke, and malaria. Despite evidence for a heritable component to sICAM-1 levels, few genetic loci have been identified so far. To comprehensively address this issue, we performed a genome-wide association analysis of sICAM-1 concentration in 22,435 apparently healthy women from the Women's Genome Health Study. While our results confirm the previously reported associations at the ABO and ICAM1 loci, four novel associations were identified in the vicinity of NFKBIK (rs3136642, P = 5.4 × 10(-9)), PNPLA3 (rs738409, P = 5.8 × 10(-9)), RELA (rs1049728, P = 2.7 × 10(-16)), and SH2B3 (rs3184504, P = 2.9 × 10(-17)). Two loci, NFKBIB and RELA, are involved in NFKB signaling pathway; PNPLA3 is known for its association with fatty liver disease; and SH3B2 has been associated with a multitude of traits and disease including myocardial infarction. These associations provide insights into the genetic regulation of sICAM-1 levels and implicate these loci in the regulation of endothelial function.Soluble ICAM-1 (sICAM-1) is an endothelium-derived inflammatory marker that has been associated with diverse conditions such as myocardial infarction, diabetes, stroke, and malaria. Despite evidence for a heritable component to sICAM-1 levels, few genetic loci have been identified so far. To comprehensively address this issue, we performed a genome-wide association analysis of sICAM-1 concentration in 22,435 apparently healthy women from the Women's Genome Health Study. While our results confirm the previously reported associations at the ABO and ICAM1 loci, four novel associations were identified in the vicinity of NFKBIK (rs3136642, P = 5.4 × 10(-9)), PNPLA3 (rs738409, P = 5.8 × 10(-9)), RELA (rs1049728, P = 2.7 × 10(-16)), and SH2B3 (rs3184504, P = 2.9 × 10(-17)). Two loci, NFKBIB and RELA, are involved in NFKB signaling pathway; PNPLA3 is known for its association with fatty liver disease; and SH3B2 has been associated with a multitude of traits and disease including myocardial infarction. These associations provide insights into the genetic regulation of sICAM-1 levels and implicate these loci in the regulation of endothelial function. Soluble ICAM-1 (sICAM-1) is an endothelium-derived inflammatory marker that has been associated with diverse conditions such as myocardial infarction, diabetes, stroke, and malaria. Despite evidence for a heritable component to sICAM-1 levels, few genetic loci have been identified so far. To comprehensively address this issue, we performed a genome-wide association analysis of sICAM-1 concentration in 22,435 apparently healthy women from the Women's Genome Health Study. While our results confirm the previously reported associations at the ABO and ICAM1 loci, four novel associations were identified in the vicinity of NFKBIK (rs3136642, P = 5.4×10-9), PNPLA3 (rs738409, P = 5.8×10-9), RELA (rs1049728, P = 2.7×10-16), and SH2B3 (rs3184504, P = 2.9×10-17). Two loci, NFKBIB and RELA, are involved in NFKB signaling pathway; PNPLA3 is known for its association with fatty liver disease; and SH3B2 has been associated with a multitude of traits and disease including myocardial infarction. These associations provide insights into the genetic regulation of sICAM-1 levels and implicate these loci in the regulation of endothelial function. |
| Audience | Academic |
| Author | Parker, Alexander N. Dehghan, Abbas Paré, Guillaume Bis, Joshua C. Chasman, Daniel I. Rose, Lynda Shiffman, Dov Ridker, Paul M. Barbalic, Maja Dupuis, Josée Benjamin, Emelia J. |
| AuthorAffiliation | 11 Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts, United States of America 9 Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, Washington, United States of America 1 Center for Cardiovascular Disease Prevention, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America 8 The Netherlands Consortium on Healthy Aging (NCHA), Leiden, The Netherlands 6 Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts, United States of America 10 Section of Preventive Medicine and Epidemiology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America 7 Department of Epidemiology, Erasmus Medical Center, Rotterdam, The Netherlands 13 Amgen, Cambridge, Massachusetts, United States of America 12 Celera, Alameda, California, United States of America 5 National Heart, Lung, and Blood Institu |
| AuthorAffiliation_xml | – name: 1 Center for Cardiovascular Disease Prevention, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America – name: University of Liège, Belgium – name: 6 Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts, United States of America – name: 8 The Netherlands Consortium on Healthy Aging (NCHA), Leiden, The Netherlands – name: 4 Human Genetics Center and Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, United States of America – name: 5 National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, Massachusetts, United States of America – name: 10 Section of Preventive Medicine and Epidemiology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America – name: 11 Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts, United States of America – name: 3 McMaster University, Hamilton, Canada – name: 12 Celera, Alameda, California, United States of America – name: 9 Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, Washington, United States of America – name: 13 Amgen, Cambridge, Massachusetts, United States of America – name: 2 Donald W. Reynolds Center for Cardiovascular Research, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America – name: 7 Department of Epidemiology, Erasmus Medical Center, Rotterdam, The Netherlands |
| Author_xml | – sequence: 1 givenname: Guillaume surname: Paré fullname: Paré, Guillaume – sequence: 2 givenname: Paul M. surname: Ridker fullname: Ridker, Paul M. – sequence: 3 givenname: Lynda surname: Rose fullname: Rose, Lynda – sequence: 4 givenname: Maja surname: Barbalic fullname: Barbalic, Maja – sequence: 5 givenname: Josée surname: Dupuis fullname: Dupuis, Josée – sequence: 6 givenname: Abbas surname: Dehghan fullname: Dehghan, Abbas – sequence: 7 givenname: Joshua C. surname: Bis fullname: Bis, Joshua C. – sequence: 8 givenname: Emelia J. surname: Benjamin fullname: Benjamin, Emelia J. – sequence: 9 givenname: Dov surname: Shiffman fullname: Shiffman, Dov – sequence: 10 givenname: Alexander N. surname: Parker fullname: Parker, Alexander N. – sequence: 11 givenname: Daniel I. surname: Chasman fullname: Chasman, Daniel I. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21533024$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2011 Public Library of Science Paré et al. 2011 2011 Paré et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Paré G, Ridker PM, Rose L, Barbalic M, Dupuis J, et al. (2011) Genome-Wide Association Analysis of Soluble ICAM-1 Concentration Reveals Novel Associations at the NFKBIK, PNPLA3, RELA, and SH2B3 Loci. PLoS Genet 7(4): e1001374. doi:10.1371/journal.pgen.1001374 |
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| SubjectTerms | ABO Blood-Group System - genetics Adaptor Proteins, Signal Transducing Algorithms Cardiovascular Disorders/Coronary Artery Disease Cell adhesion molecules Charitable foundations Cohort Studies Diagnosis Disease Epidemiology Female Gene Frequency Genetic aspects Genetic Loci Genetics Genetics and Genomics/Complex Traits Genome, Human Genome-Wide Association Study Genomes Genotype Heart Heart attack Humans I-kappa B Kinase - genetics Immunology/Genetics of the Immune System Intercellular Adhesion Molecule-1 - blood Intercellular Adhesion Molecule-1 - genetics Intracellular Signaling Peptides and Proteins Lipase - genetics Liver diseases Membrane Proteins - genetics Models, Genetic Multifactorial Inheritance Physiological aspects Polymorphism, Single Nucleotide Proteins - genetics Single nucleotide polymorphisms Stroke Stroke (Disease) Transcription Factor RelA - genetics Womens health |
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| Title | Genome-Wide Association Analysis of Soluble ICAM-1 Concentration Reveals Novel Associations at the NFKBIK, PNPLA3, RELA, and SH2B3 Loci |
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