Possible control of paternal imprinting of polymorphisms of the ADAM33 gene by epigenetic mechanisms and association with level of airway hyperresponsiveness in asthmatic children

Kopřiva, František; Godava, Marek; Marková, M; Vodička, Radek; Dusek, Ladislav; Mužík, Jiří; Schneiderova, Eva; Vrtěl, Radek; Mihál, Vladimı́r

doi:10.5507/bp.2013.025

Cited by 6 publications

(4 citation statements)

References 29 publications

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“…The value of T-int >100 is considered as significantly associated as per the Haploview tool. The result supported another study where haplotypes were found to be associated with asthma18; further, these SNPs were associated with an increased predisposition to asthma29, but no such association was found in other studies3031. In another study, rs2853209 SNP was found to be associated with asthma along with T1 (rs2280091) and F+1 SNPs of ADAM33 32.…”

Section: Discussionsupporting

confidence: 73%

Haplotype analysis of ADAM33 polymorphisms in asthma

Vishweswaraiah

Ramachandra

Jayaraj

et al. 2019

Indian Journal of Medical Research

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Background & objectives:ADAM33 is implicated as a potentially strong candidate gene for asthma and bronchial hyper-responsiveness. Many polymorphisms of ADAM33 have been studied along with ADAM33 expression in various cells of the lungs. Haplotype analysis also showed association with asthma in different populations across the world. Therefore, the aim of this study was to perform a comprehensive screening of ADAM33 polymorphisms in adult patients with asthma.Methods:Thirty five polymorphisms of ADAM33 were genotyped in 55 patients with asthma and 53 controls. The association of single nucleotide polymorphisms (SNPs) and haplotypes with phenotypes of asthma was analysed.Results:The genotype, minor allele frequency, odds ratio and Hardy–Weinberg equilibrium did not show any significant difference among cases and controls. No association was found between SNPs of ADAM33 with the severity of asthma. Correlation analysis of ADAM33 SNPs to the phenotypes, based on clinical variables and allergen sensitization, did not show significant difference. Haplotype analysis showed that rs2280090 and rs2280091 were associated with asthma in the patient group.Interpretation & conclusions:Haplotype analysis showed an association of the two SNP variations with asthma. These SNPs lead to amino acid change and are prone to phosphorylation, which may affect expression levels and protein function of ADAM33 and asthma susceptibility.

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Section: Discussionsupporting

confidence: 73%

Haplotype analysis of ADAM33 polymorphisms in asthma

Vishweswaraiah

Ramachandra

Jayaraj

et al. 2019

Indian Journal of Medical Research

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“…These differences may reflect differences in the cohort composition or methodological differences, including the use of parental reports of asthma as the outcome (vs. wheeze in our studies) and a longer follow-up to 18 years in their study (27). A recent study demonstrated that paternal imprinting of ADAM33, a gene that has been associated with asthma, was associated with the severity of airway hyperreactivity in children with asthma (28), suggesting a parent-of-origin-specific effect. However, this effect was not examined in the context of the child's sex.…”

Section: Discussionmentioning

confidence: 99%

Sex-specific risk factors for childhood wheeze and longitudinal phenotypes of wheeze

Tse

Rifas‐Shiman

Coull

et al. 2016

Journal of Allergy and Clinical Immunology

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Background While sexual dimorphism in wheeze and asthma prevalence are well documented, sex-specific risk factors for wheeze and longitudinal wheeze phenotypes have not been well elucidated. Objective Using a large pre-birth cohort, this study aimed to identify sex-specific risk factors for wheeze from birth through mid-childhood, and identify distinct longitudinal wheeze phenotypes and the sex-specific risk factors associated with these phenotypes. Methods Mothers reported child wheeze symptoms over the past year, approximately yearly on 9 occasions starting at age 1 year. We identified sex-specific predictors of wheeze, wheeze phenotypes, and sex-specific predictors of these phenotypes using generalized estimating equations, latent class mixed models, and multinomial logistic analysis, respectively. Results A total of 1623 children had information on wheeze at 1 or more time points. Paternal asthma was a stronger predictor of ever wheeze in boys (OR=2.15, 95% CI 1.74, 2.66) than in girls (OR=1.53, 95% CI 1.19, 1.96, p for sex by paternal asthma interaction=0.03), while being Black or Hispanic, birthweight for gestational age z-score, and breastfeeding duration have stronger associations among girls. We identified 3 longitudinal wheeze phenotypes: never/infrequent wheeze (74.1%), early transient wheeze (12.7%), and persistent wheeze (13.1%). Compared to never/infrequent wheeze, maternal asthma, infant bronchiolitis, and atopic dermatitis were associated with persistent wheeze in both sexes, but paternal asthma was associated with persistent wheeze in boys only (OR=4.27, 95% CI 2.33, 7.83, p for sex by paternal asthma interaction=0.02) while being Black or Hispanic was a predictor for girls only. Conclusion We identified sex-specific predictors of wheeze and longitudinal wheeze patterns, which may have important prognostic value and may allow for a more personalized approach to wheeze and asthma treatment.

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Section: Male Sexmentioning

confidence: 99%

“…This is underlined by sexual dimorphism in study-specific predictors of persistent wheeze demonstrated by effects of paternal asthma for boys 12,[17][18][19][20]23 and minority race (black or Hispanic) for girls. 17 Recent reports of paternal imprinting of ADAM33 47 and sex-specific DNA methylation patterns in the promoter region of zona pellucidabinding protein 2 (ZPBP2) 48 associated with childhood asthma lend credence the sex-specific causal mechanisms. Moreover, our metaregression results suggest that higher risk of Early-Persistent wheezing among male children may be more apparent in high-risk cohorts than in population-based studies.…”

Section: Male Sexmentioning

confidence: 99%

Childhood wheeze trajectory‐specific risk factors: A systematic review and meta‐analysis

Owora

Zhang

2020

Pediatric Allergy Immunology

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Background: There is growing interest in the use of latent trajectory methodology to identify wheeze patterns in heterogeneous populations of children. This study systematically reviewed and meta-analyzed childhood wheeze trajectory studies to identify childhood wheeze trajectory group-specific risk factors among children from birth through to adolescence. Methods: We included studies that used latent trajectory methodology to identify wheeze trajectories and associated risk factors. We searched PubMed, EMBASE, and Google Scholar from 2000 through September 30, 2019, for relevant studies. The study was conducted according to the PRISMA recommendations. Results: Thirteen cohort studies conducted in eleven high-income countries were included in our meta-analysis with the length of follow-up ranging from 3 to 18 years. Five distinct latent wheeze trajectory groups were identified: Never/Infrequent, Early-Transient, Early-Persistent, Intermediate-Onset, and Late-Onset. We found moderate-to-strong evidence that family history of asthma predicted persistent childhood wheezing among male children but with lower risk among first-born children. There was weak-to-moderate evidence for childhood atopy, male sex, short duration of breastfeeding, tobacco exposure, daycare attendance, and having siblings as risk factors for Early-Transient wheezing; except for breastfeeding, these factors were also associated with intermediate and Late-Onset wheezing with varying effect sizes in high-risk vs general population cohorts. Conclusions: Our findings confirm the consistency of wheeze trajectory groups defined by onset, peak prevalence, and duration; we also suggest a common nomenclature for future trajectory studies. With the exception of the relationship between a family history of asthma and persistent childhood wheezing, commonly suspected wheeze risk factors (childhood atopy, male sex, short duration of breastfeeding, tobacco exposure, daycare attendance, and having siblings) are not trajectory-specific and have varying effects in high-risk vs general population cohorts. Delineation of time-varying risk factor effects may be critical to the specificity of wheeze trajectory group prediction to better inform prognosis and targeted early preventive intervention among at-risk children.

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Possible control of paternal imprinting of polymorphisms of the ADAM33 gene by epigenetic mechanisms and association with level of airway hyperresponsiveness in asthmatic children

Cited by 6 publications

References 29 publications

Haplotype analysis of ADAM33 polymorphisms in asthma

Haplotype analysis of ADAM33 polymorphisms in asthma

Sex-specific risk factors for childhood wheeze and longitudinal phenotypes of wheeze

Childhood wheeze trajectory‐specific risk factors: A systematic review and meta‐analysis

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