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BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia

Little is known about the association of the BCL3-PVRL2-TOMM40 SNPs and dyslipidemia. This study was to detect 12 BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia in the Chinese Maonan population. Genotyping was performed in 1130 normal and 832 dyslipidemia partici...

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Autores principales: Miao, Liu, Yin, Rui-Xing, Pan, Shang-Ling, Yang, Shuo, Yang, De-Zhai, Lin, Wei-Xiong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5906470/
https://www.ncbi.nlm.nih.gov/pubmed/29670124
http://dx.doi.org/10.1038/s41598-018-24432-w
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author Miao, Liu
Yin, Rui-Xing
Pan, Shang-Ling
Yang, Shuo
Yang, De-Zhai
Lin, Wei-Xiong
author_facet Miao, Liu
Yin, Rui-Xing
Pan, Shang-Ling
Yang, Shuo
Yang, De-Zhai
Lin, Wei-Xiong
author_sort Miao, Liu
collection PubMed
description Little is known about the association of the BCL3-PVRL2-TOMM40 SNPs and dyslipidemia. This study was to detect 12 BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia in the Chinese Maonan population. Genotyping was performed in 1130 normal and 832 dyslipidemia participants. Generalized multifactor dimensionality reduction was used to screen the best interaction combination among SNPs and environmental exposures. Allele and genotype frequencies of the detected SNPs were different between the two groups (P < 0.05–0.001). Association of the 12 SNPs and serum lipid levels was observed (P < 0.004–0.001). Multiple-locus linkage disequilibrium was not statistically independent in the population (D’ = 0.01–0.98). The dominant model of rs8100239 and rs157580 SNPs, several haplotypes and G × G interaction haplotypes contributed to a protection, whereas the dominant model of rs10402271, rs3810143, rs519113, rs6859 SNPs, another haplotypes and G × G interaction haplotypes revealed an increased morbidity function (P < 0.05–0.001). There were significant three-locus model involving SNP-SNP, SNP-environment, haplotype-haplotype interactions (P < 0.05–0.001). The subjects carrying several genotypes and haplotypes decreased dyslipidemia risk, whereas the subjects carrying other genotypes and haplotypes increased dyslipidemia risk. The BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia were observed in the Chinese Maonan population.
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spelling pubmed-59064702018-04-30 BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia Miao, Liu Yin, Rui-Xing Pan, Shang-Ling Yang, Shuo Yang, De-Zhai Lin, Wei-Xiong Sci Rep Article Little is known about the association of the BCL3-PVRL2-TOMM40 SNPs and dyslipidemia. This study was to detect 12 BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia in the Chinese Maonan population. Genotyping was performed in 1130 normal and 832 dyslipidemia participants. Generalized multifactor dimensionality reduction was used to screen the best interaction combination among SNPs and environmental exposures. Allele and genotype frequencies of the detected SNPs were different between the two groups (P < 0.05–0.001). Association of the 12 SNPs and serum lipid levels was observed (P < 0.004–0.001). Multiple-locus linkage disequilibrium was not statistically independent in the population (D’ = 0.01–0.98). The dominant model of rs8100239 and rs157580 SNPs, several haplotypes and G × G interaction haplotypes contributed to a protection, whereas the dominant model of rs10402271, rs3810143, rs519113, rs6859 SNPs, another haplotypes and G × G interaction haplotypes revealed an increased morbidity function (P < 0.05–0.001). There were significant three-locus model involving SNP-SNP, SNP-environment, haplotype-haplotype interactions (P < 0.05–0.001). The subjects carrying several genotypes and haplotypes decreased dyslipidemia risk, whereas the subjects carrying other genotypes and haplotypes increased dyslipidemia risk. The BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia were observed in the Chinese Maonan population. Nature Publishing Group UK 2018-04-18 /pmc/articles/PMC5906470/ /pubmed/29670124 http://dx.doi.org/10.1038/s41598-018-24432-w Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Miao, Liu
Yin, Rui-Xing
Pan, Shang-Ling
Yang, Shuo
Yang, De-Zhai
Lin, Wei-Xiong
BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia
title BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia
title_full BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia
title_fullStr BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia
title_full_unstemmed BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia
title_short BCL3-PVRL2-TOMM40 SNPs, gene-gene and gene-environment interactions on dyslipidemia
title_sort bcl3-pvrl2-tomm40 snps, gene-gene and gene-environment interactions on dyslipidemia
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5906470/
https://www.ncbi.nlm.nih.gov/pubmed/29670124
http://dx.doi.org/10.1038/s41598-018-24432-w
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