Genetic susceptibility for emphysematous changes of the lung in Japanese

Antariksa, Budhi; Hiyama, Keiko; Isobe, Takeshi; Oshima, Yoshie; Hara, Hitoshi; Maeda, Hitoshi; Kohno, Nobuoki

doi:10.3892/ijmm.11.3.321

Cited by 27 publications

(61 citation statements)

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“…In controls, the allelic frequencies of both EH 113His and EH 139Arg variant were 0.24. These allelic frequencies are similar to those observed in previous studies of Caucasians (7,13,17,18), but significantly different from the Asian population (15,16,19,21,22,25).…”

Section: Resultssupporting

confidence: 78%

“…Significant associations between low EH activity genotypes and COPD risk were reported in several studies, (6,(15)(16)(17)(18) but these findings were not observed in other studies (19)(20)(21)(22). Together with the finding that EH is expressed in lung tissues (23), these data suggest that EH polymorphisms may play important roles in risk for lung diseases.…”

Section: Introductionsupporting

confidence: 62%

“…Among six Asian studies, one Chinese study (16) and one Taiwanese study (15) found that slow EH activity genotypes were a risk factor for COPD. However, two Japanese studies (19,22), a Chinese study (32), and a Korean study (25) did not find a significant association between EH genotypes and COPD risk, whereas the EH polymorphism may be related with COPD severity (15,17,22). In two Caucasian studies, performed in the United Kingdom (6), and Spain (18), reported a significant higher risk among COPD patients with slow EH genotypes.…”

Section: Discussionmentioning

confidence: 99%

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Polymorphisms for microsomal epoxide hydrolase and genetic susceptibility to COPD

Park¹,

Chen²,

Wadhwa³

et al. 2005

Int J Mol Med

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Although smoking is the major causal factor in the development of chronic obstructive pulmonary disease (COPD), only 10-20% of chronic heavy cigarette smokers develop symptomatic COPD, which suggests the presence of genetic susceptibility. The human microsomal epoxide hydrolase (EH) is a metabolizing enzyme which involves the process of numerous reactive epoxide intermediates and contains polymorphic alleles which are associated with altered EH activity and may be linked to increased risk for COPD. To determine whether the EH polymorphisms contributed to increased risk for COPD, prevalence of the EH codons 113 and 139 polymorphisms were compared between COPD patients and controls using a PCR-RFLP analysis using genomic DNA isolated from 131 COPD patients and 262 individually matched controls by age (± 5 years) among Caucasians with 1:2 ratio. Significantly increased risk for COPD was observed for subjects with the EH 113His/His genotypes (OR =2.4, 95% CI=1.1-5.1). These results were consistent with the fact that a significant trend towards increased risk was observed with predicted less protective EH codon 113 genotypes (p = 0.03, trend test). A similar association was not observed for EH codon139 polymorphism. As expected, a significant correlation between smoking dose and severity of COPD was observed (p<0.001). These results suggest that EH codon 113 polymorphism may modify risk for COPD.

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Section: Resultssupporting

confidence: 78%

Section: Introductionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

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Polymorphisms for microsomal epoxide hydrolase and genetic susceptibility to COPD

Park¹,

Chen²,

Wadhwa³

et al. 2005

Int J Mol Med

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“…[2,7,[13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28]) investigating the EPHX1 T113C and A139G polymorphisms in relation to COPD or emphysema as the primary end-point were included. Two minor studies were excluded from the analyses, because we were unable to retrieve the original papers despite contacting the corresponding authors.…”

Section: Statistical Analysesmentioning

confidence: 99%

EPHX1 polymorphisms, COPD and asthma in 47,000 individuals and in meta-analysis

Lee¹,

Nordestgaard²,

Dahl³

2010

European Respiratory Journal

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We tested the hypothesis that two well-characterised functional polymorphisms of the microsomal epoxide hydrolase gene (EPHX1), T113C and A139G, may influence susceptibility to chronic obstructive pulmonary disease (COPD) and asthma.We genotyped participants from the Copenhagen City Heart Study (n510,038) and the Copenhagen General Population Study (n537,022) for the T113C and A139G variants in the EPHX1 gene and measured lung function and recorded COPD hospitalisation and asthma and smoking history. Finally, we meta-analysed results from 19 studies including 7,489 COPD cases and 42,970 controls.The OR for spirometry-defined COPD or COPD hospitalisation did not differ from 1.0 for any of the EPHX1 genotypes or phenotypes overall, or in smokers or nonsmokers separately (p-value for trend 0.18-0.91). Likewise, EPHX1 genotypes or phenotypes did not associate with risk of asthma (p-value for trend 0.46-0.98). In meta-analysis, random effects OR for COPD in T113C heterozygotes and homozygotes versus non-carriers were 1.17 (0.99-1.38) and 1.38 (1.09-1.74), respectively. Corresponding values for A139G were 0.93 (0.83-1.05) and 0.89 (0.78-1.02).Our results indicate that genetically reduced microsomal epoxide hydrolase activity is not a major risk factor for COPD or asthma in the Danish population; however, meta-analysis cannot completely exclude a minor effect on COPD risk.

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“…These studies included 9 Caucasian populations (Rodriguez et al, 2002;Korytina et al, 2003;Hersh et al, 2005;Park et al, 2005;Brøgger et al, 2006;Chappell et al, 2008;Židzik et al, 2008;Penyige et al, 2010;Lee et al, 2011) and 10 Eastern Asian populations (Takeyabu et al, 2000;Yim et al, 2000;Yoshikawa et al, 2000;Zhang et al, 2002;Budhi et al, 2003;Park et al, 2003;Cheng et al, 2004;Xiao et al, 2004;Fu et al, 2007;Hua et al, 2012) ( Table 1). The total number of samples in the Caucasian and Eastern Asian populations were 47,048 (6471 cases vs 40,577 controls) and 2586 (1228 cases vs 1358 controls), respectively.…”

Section: Literature Searchmentioning

confidence: 99%

Exploration of association between EPHX1 and chronic obstructive pulmonary disease on the basis of combined data mining

Liu¹,

Xia²,

Zhou³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Chronic obstructive pulmonary disease (COPD) is an important respiratory disease with high mortality. Although smoking is the major environmental risk factor for the development of COPD, only 10% of heavy smokers develop symptomatic disease, suggesting association between genetic susceptibilities and environmental influences. In recent years, as one of the most widely studied genes including tests for associations between a genetic variant and COPD, epoxide hydrolase 1 (EPHX1) was found to be involved in the metabolism of tobacco smoke, an important risk factor of COPD. However, genetic associations with COPD identified in studies on EPHX1 are controversial. To address this issue, except for performing the meta-analysis, which specially added our current study on two polymorphisms (T337C and A416G) of EPHX1, we performed combined data mining based on functional prediction algorithms of nonsynonymous single-nucleotide polymorphisms and gene-based variable threshold testing. Genetic variations in EPHX1 did not affect COPD in Caucasian and Eastern Asian population, which is supported by recent evidence. We found no association between EPHX1 and COPD; however, a minor effect of EPHX1 on COPD risk was not completely excluded; further replication studies with large samples are needed to confirm our findings.

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Genetic susceptibility for emphysematous changes of the lung in Japanese

Cited by 27 publications

References 0 publications

Polymorphisms for microsomal epoxide hydrolase and genetic susceptibility to COPD

Polymorphisms for microsomal epoxide hydrolase and genetic susceptibility to COPD

EPHX1 polymorphisms, COPD and asthma in 47,000 individuals and in meta-analysis

Exploration of association between EPHX1 and chronic obstructive pulmonary disease on the basis of combined data mining

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