The rs7044343 Polymorphism of the Interleukin 33 Gene Is Associated with Decreased Risk of Developing Premature Coronary Artery Disease and Central Obesity, and Could Be Involved in Regulating the Production of IL-33
The effect of interleukin 33 (IL-33) in the inflammatory process generates significant interest in the potential significance of IL-33 as a biomarker for coronary artery disease (CAD). Here, our objective was to analyze whether IL-33 gene polymorphisms are associated with premature CAD in a case-con...
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Veröffentlicht in: | PloS one 2017-01, Vol.12 (1), p.e0168828-e0168828 |
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creator | Angeles-Martínez, Javier Posadas-Sánchez, Rosalinda Llorente, Luis Alvarez-León, Edith Ramírez-Bello, Julian Villarreal-Molina, Teresa Lima, Guadalupe Cardoso-Saldaña, Guillermo Rodríguez-Pérez, José Manuel Pérez-Hernández, Nonanzit Fragoso, José Manuel Posadas-Romero, Carlos Vargas-Alarcón, Gilberto |
description | The effect of interleukin 33 (IL-33) in the inflammatory process generates significant interest in the potential significance of IL-33 as a biomarker for coronary artery disease (CAD). Here, our objective was to analyze whether IL-33 gene polymorphisms are associated with premature CAD in a case-control association study.
Four IL-33 polymorphisms (rs7848215, rs16924144, rs16924159 and rs7044343) were genotyped by 5' exonuclease TaqMan assays in 1095 patients with premature CAD and 1118 controls.
The rs7044343 T allele was significantly associated with a diminished risk of premature CAD (OR = 0.81, 95% CI: 0.69-0.97, Pdom = 0.020; OR = 0.85, 95% CI: 0.75-0.96, Padd = 0.019) and central obesity (OR = 0.74, 95% CI: 0.58-0.93, Pdom = 0.0007), respectively. When patients were divided into groups with and without type 2 diabetes mellitus (T2DM), the rs7044343 T allele was associated with a reduced risk of premature CAD in patients without (OR = 0.85, 95% CI: 0.73-0.99, Padd = 0.038) and with T2DM (OR = 0.61, 95% CI: 0.38-0.97, Pdom = 0.039; OR = 0.69, 95% CI: 0.49-0.97, Padd = 0.035). In order to establish the functional effect of the rs7044343 polymorphism, the production of IL-33 was determined in monocytes of selected individuals. Monocytes from individuals with rs7044343 CC genotype produced higher levels of IL-33 than monocytes from individuals with other genotypes.
The results suggest that the IL-33 rs7044343 T allele could be a susceptibility marker for premature CAD and central obesity. The rs7044343 polymorphism could be involved in regulating the production of IL-33. |
doi_str_mv | 10.1371/journal.pone.0168828 |
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Four IL-33 polymorphisms (rs7848215, rs16924144, rs16924159 and rs7044343) were genotyped by 5' exonuclease TaqMan assays in 1095 patients with premature CAD and 1118 controls.
The rs7044343 T allele was significantly associated with a diminished risk of premature CAD (OR = 0.81, 95% CI: 0.69-0.97, Pdom = 0.020; OR = 0.85, 95% CI: 0.75-0.96, Padd = 0.019) and central obesity (OR = 0.74, 95% CI: 0.58-0.93, Pdom = 0.0007), respectively. When patients were divided into groups with and without type 2 diabetes mellitus (T2DM), the rs7044343 T allele was associated with a reduced risk of premature CAD in patients without (OR = 0.85, 95% CI: 0.73-0.99, Padd = 0.038) and with T2DM (OR = 0.61, 95% CI: 0.38-0.97, Pdom = 0.039; OR = 0.69, 95% CI: 0.49-0.97, Padd = 0.035). In order to establish the functional effect of the rs7044343 polymorphism, the production of IL-33 was determined in monocytes of selected individuals. Monocytes from individuals with rs7044343 CC genotype produced higher levels of IL-33 than monocytes from individuals with other genotypes.
The results suggest that the IL-33 rs7044343 T allele could be a susceptibility marker for premature CAD and central obesity. The rs7044343 polymorphism could be involved in regulating the production of IL-33.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0168828</identifier><identifier>PMID: 28045954</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Alcohol use ; Alleles ; Analysis ; Arthritis ; Atherosclerosis ; Authorship ; Biology and Life Sciences ; Biomarkers ; Cardiovascular disease ; Case-Control Studies ; Control methods ; Coronary artery ; Coronary artery disease ; Coronary Artery Disease - genetics ; Coronary heart disease ; Coronary vessels ; Cytokines ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Endocrinology ; Exonuclease ; Female ; Gene expression ; Gene polymorphism ; Genetic aspects ; Genetic Markers - genetics ; Genetic polymorphisms ; Genetic Predisposition to Disease ; Genotypes ; Health risks ; Heart diseases ; Humans ; Immunology ; Inflammation ; Interleukin ; Interleukin-33 - genetics ; Interleukins ; Laboratories ; Male ; Medicine and Health Sciences ; Metabolism ; Middle Aged ; Molecular biology ; Monocytes ; Monocytes - metabolism ; Multiculturalism & pluralism ; Obesity ; Obesity, Abdominal - genetics ; Patients ; Polymorphism ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Population ; Rheumatology ; Risk ; Risk factors ; Tomography, X-Ray Computed</subject><ispartof>PloS one, 2017-01, Vol.12 (1), p.e0168828-e0168828</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Angeles-Martínez et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Angeles-Martínez et al 2017 Angeles-Martínez et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-f9d2bded8acc43eb6c39a890098cd33379118f18650820ee1f6cde532a51ed863</citedby><cites>FETCH-LOGICAL-c725t-f9d2bded8acc43eb6c39a890098cd33379118f18650820ee1f6cde532a51ed863</cites><orcidid>0000-0001-7916-5163</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5207498/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5207498/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28045954$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Lin, Ying-Ju</contributor><creatorcontrib>Angeles-Martínez, Javier</creatorcontrib><creatorcontrib>Posadas-Sánchez, Rosalinda</creatorcontrib><creatorcontrib>Llorente, Luis</creatorcontrib><creatorcontrib>Alvarez-León, Edith</creatorcontrib><creatorcontrib>Ramírez-Bello, Julian</creatorcontrib><creatorcontrib>Villarreal-Molina, Teresa</creatorcontrib><creatorcontrib>Lima, Guadalupe</creatorcontrib><creatorcontrib>Cardoso-Saldaña, Guillermo</creatorcontrib><creatorcontrib>Rodríguez-Pérez, José Manuel</creatorcontrib><creatorcontrib>Pérez-Hernández, Nonanzit</creatorcontrib><creatorcontrib>Fragoso, José Manuel</creatorcontrib><creatorcontrib>Posadas-Romero, Carlos</creatorcontrib><creatorcontrib>Vargas-Alarcón, Gilberto</creatorcontrib><title>The rs7044343 Polymorphism of the Interleukin 33 Gene Is Associated with Decreased Risk of Developing Premature Coronary Artery Disease and Central Obesity, and Could Be Involved in Regulating the Production of IL-33</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The effect of interleukin 33 (IL-33) in the inflammatory process generates significant interest in the potential significance of IL-33 as a biomarker for coronary artery disease (CAD). Here, our objective was to analyze whether IL-33 gene polymorphisms are associated with premature CAD in a case-control association study.
Four IL-33 polymorphisms (rs7848215, rs16924144, rs16924159 and rs7044343) were genotyped by 5' exonuclease TaqMan assays in 1095 patients with premature CAD and 1118 controls.
The rs7044343 T allele was significantly associated with a diminished risk of premature CAD (OR = 0.81, 95% CI: 0.69-0.97, Pdom = 0.020; OR = 0.85, 95% CI: 0.75-0.96, Padd = 0.019) and central obesity (OR = 0.74, 95% CI: 0.58-0.93, Pdom = 0.0007), respectively. When patients were divided into groups with and without type 2 diabetes mellitus (T2DM), the rs7044343 T allele was associated with a reduced risk of premature CAD in patients without (OR = 0.85, 95% CI: 0.73-0.99, Padd = 0.038) and with T2DM (OR = 0.61, 95% CI: 0.38-0.97, Pdom = 0.039; OR = 0.69, 95% CI: 0.49-0.97, Padd = 0.035). In order to establish the functional effect of the rs7044343 polymorphism, the production of IL-33 was determined in monocytes of selected individuals. Monocytes from individuals with rs7044343 CC genotype produced higher levels of IL-33 than monocytes from individuals with other genotypes.
The results suggest that the IL-33 rs7044343 T allele could be a susceptibility marker for premature CAD and central obesity. The rs7044343 polymorphism could be involved in regulating the production of IL-33.</description><subject>Adult</subject><subject>Alcohol use</subject><subject>Alleles</subject><subject>Analysis</subject><subject>Arthritis</subject><subject>Atherosclerosis</subject><subject>Authorship</subject><subject>Biology and Life Sciences</subject><subject>Biomarkers</subject><subject>Cardiovascular disease</subject><subject>Case-Control Studies</subject><subject>Control methods</subject><subject>Coronary artery</subject><subject>Coronary artery disease</subject><subject>Coronary Artery Disease - genetics</subject><subject>Coronary heart disease</subject><subject>Coronary vessels</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Endocrinology</subject><subject>Exonuclease</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene polymorphism</subject><subject>Genetic aspects</subject><subject>Genetic Markers - genetics</subject><subject>Genetic polymorphisms</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotypes</subject><subject>Health risks</subject><subject>Heart diseases</subject><subject>Humans</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Interleukin</subject><subject>Interleukin-33 - genetics</subject><subject>Interleukins</subject><subject>Laboratories</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Molecular biology</subject><subject>Monocytes</subject><subject>Monocytes - metabolism</subject><subject>Multiculturalism & pluralism</subject><subject>Obesity</subject><subject>Obesity, Abdominal - genetics</subject><subject>Patients</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Population</subject><subject>Rheumatology</subject><subject>Risk</subject><subject>Risk factors</subject><subject>Tomography, X-Ray 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rs7044343 Polymorphism of the Interleukin 33 Gene Is Associated with Decreased Risk of Developing Premature Coronary Artery Disease and Central Obesity, and Could Be Involved in Regulating the Production of IL-33</title><author>Angeles-Martínez, Javier ; Posadas-Sánchez, Rosalinda ; Llorente, Luis ; Alvarez-León, Edith ; Ramírez-Bello, Julian ; Villarreal-Molina, Teresa ; Lima, Guadalupe ; Cardoso-Saldaña, Guillermo ; Rodríguez-Pérez, José Manuel ; Pérez-Hernández, Nonanzit ; Fragoso, José Manuel ; Posadas-Romero, Carlos ; Vargas-Alarcón, Gilberto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c725t-f9d2bded8acc43eb6c39a890098cd33379118f18650820ee1f6cde532a51ed863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Alcohol 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diseases</topic><topic>Humans</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Interleukin</topic><topic>Interleukin-33 - genetics</topic><topic>Interleukins</topic><topic>Laboratories</topic><topic>Male</topic><topic>Medicine and Health Sciences</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>Molecular biology</topic><topic>Monocytes</topic><topic>Monocytes - metabolism</topic><topic>Multiculturalism & pluralism</topic><topic>Obesity</topic><topic>Obesity, Abdominal - genetics</topic><topic>Patients</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Population</topic><topic>Rheumatology</topic><topic>Risk</topic><topic>Risk factors</topic><topic>Tomography, X-Ray Computed</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Angeles-Martínez, Javier</creatorcontrib><creatorcontrib>Posadas-Sánchez, 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Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Angeles-Martínez, Javier</au><au>Posadas-Sánchez, Rosalinda</au><au>Llorente, Luis</au><au>Alvarez-León, Edith</au><au>Ramírez-Bello, Julian</au><au>Villarreal-Molina, Teresa</au><au>Lima, Guadalupe</au><au>Cardoso-Saldaña, Guillermo</au><au>Rodríguez-Pérez, José Manuel</au><au>Pérez-Hernández, Nonanzit</au><au>Fragoso, José Manuel</au><au>Posadas-Romero, Carlos</au><au>Vargas-Alarcón, Gilberto</au><au>Lin, Ying-Ju</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The rs7044343 Polymorphism of the Interleukin 33 Gene Is Associated with Decreased Risk of Developing Premature Coronary Artery Disease and Central Obesity, and Could Be Involved in Regulating the Production of IL-33</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-01-03</date><risdate>2017</risdate><volume>12</volume><issue>1</issue><spage>e0168828</spage><epage>e0168828</epage><pages>e0168828-e0168828</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The effect of interleukin 33 (IL-33) in the inflammatory process generates significant interest in the potential significance of IL-33 as a biomarker for coronary artery disease (CAD). Here, our objective was to analyze whether IL-33 gene polymorphisms are associated with premature CAD in a case-control association study.
Four IL-33 polymorphisms (rs7848215, rs16924144, rs16924159 and rs7044343) were genotyped by 5' exonuclease TaqMan assays in 1095 patients with premature CAD and 1118 controls.
The rs7044343 T allele was significantly associated with a diminished risk of premature CAD (OR = 0.81, 95% CI: 0.69-0.97, Pdom = 0.020; OR = 0.85, 95% CI: 0.75-0.96, Padd = 0.019) and central obesity (OR = 0.74, 95% CI: 0.58-0.93, Pdom = 0.0007), respectively. When patients were divided into groups with and without type 2 diabetes mellitus (T2DM), the rs7044343 T allele was associated with a reduced risk of premature CAD in patients without (OR = 0.85, 95% CI: 0.73-0.99, Padd = 0.038) and with T2DM (OR = 0.61, 95% CI: 0.38-0.97, Pdom = 0.039; OR = 0.69, 95% CI: 0.49-0.97, Padd = 0.035). In order to establish the functional effect of the rs7044343 polymorphism, the production of IL-33 was determined in monocytes of selected individuals. Monocytes from individuals with rs7044343 CC genotype produced higher levels of IL-33 than monocytes from individuals with other genotypes.
The results suggest that the IL-33 rs7044343 T allele could be a susceptibility marker for premature CAD and central obesity. The rs7044343 polymorphism could be involved in regulating the production of IL-33.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28045954</pmid><doi>10.1371/journal.pone.0168828</doi><tpages>e0168828</tpages><orcidid>https://orcid.org/0000-0001-7916-5163</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2017-01, Vol.12 (1), p.e0168828-e0168828 |
issn | 1932-6203 1932-6203 |
language | eng |
recordid | cdi_plos_journals_1855068934 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
subjects | Adult Alcohol use Alleles Analysis Arthritis Atherosclerosis Authorship Biology and Life Sciences Biomarkers Cardiovascular disease Case-Control Studies Control methods Coronary artery Coronary artery disease Coronary Artery Disease - genetics Coronary heart disease Coronary vessels Cytokines Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Endocrinology Exonuclease Female Gene expression Gene polymorphism Genetic aspects Genetic Markers - genetics Genetic polymorphisms Genetic Predisposition to Disease Genotypes Health risks Heart diseases Humans Immunology Inflammation Interleukin Interleukin-33 - genetics Interleukins Laboratories Male Medicine and Health Sciences Metabolism Middle Aged Molecular biology Monocytes Monocytes - metabolism Multiculturalism & pluralism Obesity Obesity, Abdominal - genetics Patients Polymorphism Polymorphism, Genetic Polymorphism, Single Nucleotide Population Rheumatology Risk Risk factors Tomography, X-Ray Computed |
title | The rs7044343 Polymorphism of the Interleukin 33 Gene Is Associated with Decreased Risk of Developing Premature Coronary Artery Disease and Central Obesity, and Could Be Involved in Regulating the Production of IL-33 |
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