Exploring epistatic relationships of NO biosynthesis pathway genes in susceptibility to CHD
Aim： To assess the epistatic relationships of nitric oxide （NO） biosynthesis pathway genes in susceptibility to coronary heart disease （CHD）. Methods： A total of 2142 subjects enrolled in two case-control studies was genotyped for 7 single-nucleotide polymorphisms （SNP） within NO biosynthesis pathwa...
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| Veröffentlicht in: | Acta pharmacologica Sinica 2010-07, Vol.31 (7), p.874-880 |
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| creator | Tu, Yuan-chao Ding, Hu Wang, Xiao-jing Xu, Yu-jun Zhang, Lan Huang, Cong-xin Wang, Dao-wen |
| description | Aim： To assess the epistatic relationships of nitric oxide （NO） biosynthesis pathway genes in susceptibility to coronary heart disease （CHD）. Methods： A total of 2142 subjects enrolled in two case-control studies was genotyped for 7 single-nucleotide polymorphisms （SNP） within NO biosynthesis pathway genes using TaqMan assays. The association analyses were performed at both SNP and haplotype levels. Two-way SNP-SNP interactions and high-order interactions were tested using multiple unconditional logistic regression analyses and generalized multifactor dimensionality reduction （GMDR） analyses, respectively. Results： Two alleles （rs1049255＊C and rs841＊A） were identified that were significantly associated with increased risk of CHD after adjusting for all confounders （0R=1.21, 95% CI： 1.06-1.39, combined P=0.001, Poorr=0.007 and 0R=1.30, 95% CI 1.12-1.50, combined P〈0.001, Pcorr〈0.001, respectively）. Significant two-way SNP-SNP interactions were found between SNP rs2297518 and these two significant polyrnorphisms, affecting the risk of CHD （P〈0.001 for both）. No significant high-order interactions were identified. Conclusion： The results suggested that two-way SNP-SNP interactions of potymorphisms within NO biosynthesis pathway genes contribute to CHD risk. |
| doi_str_mv | 10.1038/aps.2010.68 |
| format | Article |
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Methods： A total of 2142 subjects enrolled in two case-control studies was genotyped for 7 single-nucleotide polymorphisms （SNP） within NO biosynthesis pathway genes using TaqMan assays. The association analyses were performed at both SNP and haplotype levels. Two-way SNP-SNP interactions and high-order interactions were tested using multiple unconditional logistic regression analyses and generalized multifactor dimensionality reduction （GMDR） analyses, respectively. Results： Two alleles （rs1049255＊C and rs841＊A） were identified that were significantly associated with increased risk of CHD after adjusting for all confounders （0R=1.21, 95% CI： 1.06-1.39, combined P=0.001, Poorr=0.007 and 0R=1.30, 95% CI 1.12-1.50, combined P〈0.001, Pcorr〈0.001, respectively）. Significant two-way SNP-SNP interactions were found between SNP rs2297518 and these two significant polyrnorphisms, affecting the risk of CHD （P〈0.001 for both）. No significant high-order interactions were identified. Conclusion： The results suggested that two-way SNP-SNP interactions of potymorphisms within NO biosynthesis pathway genes contribute to CHD risk.</description><identifier>ISSN: 1671-4083</identifier><identifier>EISSN: 1745-7254</identifier><identifier>DOI: 10.1038/aps.2010.68</identifier><identifier>PMID: 20581851</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Aged ; Alleles ; Asian Continental Ancestry Group - genetics ; Biomedical and Life Sciences ; Biomedicine ; Case-Control Studies ; China ; Coronary Disease - genetics ; Epistasis, Genetic ; Female ; Genetic Predisposition to Disease ; GTP Cyclohydrolase - genetics ; Haplotypes ; Humans ; Immunology ; Internal Medicine ; Logistic Models ; logistic回归分析 ; Male ; Medical Microbiology ; Middle Aged ; NADPH Oxidases - genetics ; Nitric Oxide - biosynthesis ; Nitric Oxide - genetics ; Original ; original-article ; Pharmacology/Toxicology ; Polymorphism, Single Nucleotide ; Vaccine ; 一氧化氮合成 ; 冠心病 ; 单核苷酸多态性 ; 基因分型 ; 易感性 ; 生物合成途径</subject><ispartof>Acta pharmacologica Sinica, 2010-07, Vol.31 (7), p.874-880</ispartof><rights>CPS and SIMM 2010</rights><rights>Copyright Nature Publishing Group Jul 2010</rights><rights>Copyright © 2010 CPS and SIMM 2010 CPS and SIMM</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-2e1a54f2d91a8c9a0b1a3519dc04c878a277822d4632eab5acb84f9380ce5feb3</citedby><cites>FETCH-LOGICAL-c471t-2e1a54f2d91a8c9a0b1a3519dc04c878a277822d4632eab5acb84f9380ce5feb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/95561A/95561A.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007729/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007729/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20581851$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tu, Yuan-chao</creatorcontrib><creatorcontrib>Ding, Hu</creatorcontrib><creatorcontrib>Wang, Xiao-jing</creatorcontrib><creatorcontrib>Xu, Yu-jun</creatorcontrib><creatorcontrib>Zhang, Lan</creatorcontrib><creatorcontrib>Huang, Cong-xin</creatorcontrib><creatorcontrib>Wang, Dao-wen</creatorcontrib><title>Exploring epistatic relationships of NO biosynthesis pathway genes in susceptibility to CHD</title><title>Acta pharmacologica Sinica</title><addtitle>Acta Pharmacol Sin</addtitle><addtitle>Acta Pharmacologica Sinica</addtitle><description>Aim： To assess the epistatic relationships of nitric oxide （NO） biosynthesis pathway genes in susceptibility to coronary heart disease （CHD）. Methods： A total of 2142 subjects enrolled in two case-control studies was genotyped for 7 single-nucleotide polymorphisms （SNP） within NO biosynthesis pathway genes using TaqMan assays. The association analyses were performed at both SNP and haplotype levels. Two-way SNP-SNP interactions and high-order interactions were tested using multiple unconditional logistic regression analyses and generalized multifactor dimensionality reduction （GMDR） analyses, respectively. Results： Two alleles （rs1049255＊C and rs841＊A） were identified that were significantly associated with increased risk of CHD after adjusting for all confounders （0R=1.21, 95% CI： 1.06-1.39, combined P=0.001, Poorr=0.007 and 0R=1.30, 95% CI 1.12-1.50, combined P〈0.001, Pcorr〈0.001, respectively）. Significant two-way SNP-SNP interactions were found between SNP rs2297518 and these two significant polyrnorphisms, affecting the risk of CHD （P〈0.001 for both）. No significant high-order interactions were identified. Conclusion： The results suggested that two-way SNP-SNP interactions of potymorphisms within NO biosynthesis pathway genes contribute to CHD risk.</description><subject>Aged</subject><subject>Alleles</subject><subject>Asian Continental Ancestry Group - genetics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Case-Control Studies</subject><subject>China</subject><subject>Coronary Disease - genetics</subject><subject>Epistasis, Genetic</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>GTP Cyclohydrolase - genetics</subject><subject>Haplotypes</subject><subject>Humans</subject><subject>Immunology</subject><subject>Internal Medicine</subject><subject>Logistic Models</subject><subject>logistic回归分析</subject><subject>Male</subject><subject>Medical Microbiology</subject><subject>Middle Aged</subject><subject>NADPH Oxidases - genetics</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide - genetics</subject><subject>Original</subject><subject>original-article</subject><subject>Pharmacology/Toxicology</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Vaccine</subject><subject>一氧化氮合成</subject><subject>冠心病</subject><subject>单核苷酸多态性</subject><subject>基因分型</subject><subject>易感性</subject><subject>生物合成途径</subject><issn>1671-4083</issn><issn>1745-7254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkb1vFDEQxS1EREKgokcWDQVs8Ofa20RCl0AiRaSBisLy-ry3Dnu2Y3sh99_j010CQVTjkX_z5o0eAK8wOsGIyg865hOCatfKJ-AIC8YbQTh7Wt-twA1Dkh6C5znfIEQJxd0zcEgQl1hyfAS-n9_FKSTnV9BGl4suzsBkp1qDz6OLGYYBfrmGvQt548tos8sw6jL-0hu4st5m6DzMczY2Fte7yZUNLAEuLs5egINBT9m-3Ndj8O3T-dfFRXN1_fly8fGqMUzg0hCLNWcDWXZYS9Np1GNNOe6WBjEjhdRECEnIkrWUWN1zbXrJho5KZCwfbE-PwelON8792i6N9SXpScXk1jptVNBOPf7xblSr8FMxhIQgXRV4uxdI4Xa2uai1q_dMk_Y2zFkJSluKGGGVfPMPeRPm5Ot1igtJERZcVujdDjIp5Jzs8GAFI7WNTNXI1DYy1W7p13-7f2DvM6rA-x2Q4zYnm_7s_L_e3qIZg1_d1gnVa_NjcJNVlLUESyLob0cnre8</recordid><startdate>20100701</startdate><enddate>20100701</enddate><creator>Tu, Yuan-chao</creator><creator>Ding, Hu</creator><creator>Wang, Xiao-jing</creator><creator>Xu, Yu-jun</creator><creator>Zhang, Lan</creator><creator>Huang, Cong-xin</creator><creator>Wang, Dao-wen</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W94</scope><scope>WU4</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100701</creationdate><title>Exploring epistatic relationships of NO biosynthesis pathway genes in susceptibility to CHD</title><author>Tu, Yuan-chao ; Ding, Hu ; Wang, Xiao-jing ; Xu, Yu-jun ; Zhang, Lan ; Huang, Cong-xin ; Wang, Dao-wen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-2e1a54f2d91a8c9a0b1a3519dc04c878a277822d4632eab5acb84f9380ce5feb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Aged</topic><topic>Alleles</topic><topic>Asian Continental Ancestry Group - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta pharmacologica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tu, Yuan-chao</au><au>Ding, Hu</au><au>Wang, Xiao-jing</au><au>Xu, Yu-jun</au><au>Zhang, Lan</au><au>Huang, Cong-xin</au><au>Wang, Dao-wen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exploring epistatic relationships of NO biosynthesis pathway genes in susceptibility to CHD</atitle><jtitle>Acta pharmacologica Sinica</jtitle><stitle>Acta Pharmacol Sin</stitle><addtitle>Acta Pharmacologica Sinica</addtitle><date>2010-07-01</date><risdate>2010</risdate><volume>31</volume><issue>7</issue><spage>874</spage><epage>880</epage><pages>874-880</pages><issn>1671-4083</issn><eissn>1745-7254</eissn><abstract>Aim： To assess the epistatic relationships of nitric oxide （NO） biosynthesis pathway genes in susceptibility to coronary heart disease （CHD）. Methods： A total of 2142 subjects enrolled in two case-control studies was genotyped for 7 single-nucleotide polymorphisms （SNP） within NO biosynthesis pathway genes using TaqMan assays. The association analyses were performed at both SNP and haplotype levels. Two-way SNP-SNP interactions and high-order interactions were tested using multiple unconditional logistic regression analyses and generalized multifactor dimensionality reduction （GMDR） analyses, respectively. Results： Two alleles （rs1049255＊C and rs841＊A） were identified that were significantly associated with increased risk of CHD after adjusting for all confounders （0R=1.21, 95% CI： 1.06-1.39, combined P=0.001, Poorr=0.007 and 0R=1.30, 95% CI 1.12-1.50, combined P〈0.001, Pcorr〈0.001, respectively）. Significant two-way SNP-SNP interactions were found between SNP rs2297518 and these two significant polyrnorphisms, affecting the risk of CHD （P〈0.001 for both）. No significant high-order interactions were identified. Conclusion： The results suggested that two-way SNP-SNP interactions of potymorphisms within NO biosynthesis pathway genes contribute to CHD risk.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>20581851</pmid><doi>10.1038/aps.2010.68</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Alleles Asian Continental Ancestry Group - genetics Biomedical and Life Sciences Biomedicine Case-Control Studies China Coronary Disease - genetics Epistasis, Genetic Female Genetic Predisposition to Disease GTP Cyclohydrolase - genetics Haplotypes Humans Immunology Internal Medicine Logistic Models logistic回归分析 Male Medical Microbiology Middle Aged NADPH Oxidases - genetics Nitric Oxide - biosynthesis Nitric Oxide - genetics Original original-article Pharmacology/Toxicology Polymorphism, Single Nucleotide Vaccine 一氧化氮合成 冠心病 单核苷酸多态性 基因分型 易感性 生物合成途径 |
| title | Exploring epistatic relationships of NO biosynthesis pathway genes in susceptibility to CHD |
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