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4 results on '"Boezen, H. M. (H Marike)"'

1. A cross-omics integrative study of metabolic signatures of chronic obstructive pulmonary disease

Author

Prokić, I. (Ivana), Lahousse, L. (Lies), de Vries, M. (Maaike), Liu, J. (Jun), Kalaoja, M. (Marita), Vonk, J. M. (Judith M.), van der Plaat, D. A. (Diana A.), van Diemen, C. C. (Cleo C.), van der Spek, A. (Ashley), Zhernakova, A. (Alexandra), Fu, J. (Jingyuan), Ghanbari, M. (Mohsen), Ala-Korpela, M. (Mika), Kettunen, J. (Johannes), Havulinna, A. S. (Aki S.), Perola, M. (Markus), Salomaa, V. (Veikko), Lind, L. (Lars), Ärnlöv, J. (Johan), Stricker, B. H. (Bruno H. C.), Brusselle, G. G. (Guy G.), Boezen, H. M. (H. Marike), van Duijn, C. M. (Cornelia M.), Amin, N. (Najaf), Prokić, I. (Ivana), Lahousse, L. (Lies), de Vries, M. (Maaike), Liu, J. (Jun), Kalaoja, M. (Marita), Vonk, J. M. (Judith M.), van der Plaat, D. A. (Diana A.), van Diemen, C. C. (Cleo C.), van der Spek, A. (Ashley), Zhernakova, A. (Alexandra), Fu, J. (Jingyuan), Ghanbari, M. (Mohsen), Ala-Korpela, M. (Mika), Kettunen, J. (Johannes), Havulinna, A. S. (Aki S.), Perola, M. (Markus), Salomaa, V. (Veikko), Lind, L. (Lars), Ärnlöv, J. (Johan), Stricker, B. H. (Bruno H. C.), Brusselle, G. G. (Guy G.), Boezen, H. M. (H. Marike), van Duijn, C. M. (Cornelia M.), and Amin, N. (Najaf)

Abstract

Background: Chronic obstructive pulmonary disease (COPD) is a common lung disorder characterized by persistent and progressive airflow limitation as well as systemic changes. Metabolic changes in blood may help detect COPD in an earlier stage and predict prognosis. Methods: We conducted a comprehensive study of circulating metabolites, measured by proton Nuclear Magnetic Resonance Spectroscopy, in relation with COPD and lung function. The discovery sample consisted of 5557 individuals from two large population-based studies in the Netherlands, the Rotterdam Study and the Erasmus Rucphen Family study. Significant findings were replicated in 12,205 individuals from the Lifelines-DEEP study, FINRISK and the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) studies. For replicated metabolites further investigation of causality was performed, utilizing genetics in the Mendelian randomization approach. Results: There were 602 cases of COPD and 4955 controls used in the discovery meta-analysis. Our logistic regression results showed that higher levels of plasma Glycoprotein acetyls (GlycA) are significantly associated with COPD (OR = 1.16, P = 5.6 × 10⁻⁴ in the discovery and OR = 1.30, P = 1.8 × 10⁻⁶ in the replication sample). A bi-directional two-sample Mendelian randomization analysis suggested that circulating blood GlycA is not causally related to COPD, but that COPD causally increases GlycA levels. Using the prospective data of the same sample of Rotterdam Study in Cox-regression, we show that the circulating GlycA level is a predictive biomarker of COPD incidence (HR = 1.99, 95%CI 1.52–2.60, comparing those in the highest and lowest quartile of GlycA) but is not significantly associated with mortality in COPD patients (HR = 1.07, 95%CI 0.94–1.20). Conclusions: Our study shows that circulating blood GlycA is a biomarker of early COPD pathology.

Published
2020

2. Epigenome-wide association study of lung function level and its change

Author

Imboden, M. (Medea), Wielscher, M. (Matthias), Rezwan, F. I. (Faisal I.), Amaral, A. F. (André F.S.), Schaffner, E. (Emmanuel), Jeong, A. (Ayoung), Beckmeyer-Borowko, A. (Anna), Harris, S. E. (Sarah E.), Starr, J. M. (John M.), Deary, I. J. (Ian J.), Flexeder, C. (Claudia), Waldenberger, M. (Melanie), Peters, A. (Annette), Schulz, H. (Holger), Chen, S. (Su), Sunny, S. K. (Shadia Khan), Karmaus, W. J. (Wilfried J.J.), Jiang, Y. (Yu), Erhart, G. (Gertraud), Kronenberg, F. (Florian), Arathimos, R. (Ryan), Sharp, G. C. (Gemma C.), Henderson, A. J. (Alexander John), Fu, Y. (Yu), Piirilä, P. (Päivi), Pietiläinen, K. H. (Kirsi H.), Ollikainen, M. (Miina), Johansson, A. (Asa), Gyllensten, U. (Ulf), de Vries, M. (Maaike), van der Plaat, D. A. (Diana A.), de Jong, K. (Kim), Boezen, H. M. (H. Marike), Hall, I. P. (Ian P.), Tobin, M. D. (Martin D.), Jarvelin, M.-R. (Marjo-Riitta), Holloway, J. W. (John W.), Jarvis, D. (Deborah), Probst-Hensch, N. M. (Nicole M.), Imboden, M. (Medea), Wielscher, M. (Matthias), Rezwan, F. I. (Faisal I.), Amaral, A. F. (André F.S.), Schaffner, E. (Emmanuel), Jeong, A. (Ayoung), Beckmeyer-Borowko, A. (Anna), Harris, S. E. (Sarah E.), Starr, J. M. (John M.), Deary, I. J. (Ian J.), Flexeder, C. (Claudia), Waldenberger, M. (Melanie), Peters, A. (Annette), Schulz, H. (Holger), Chen, S. (Su), Sunny, S. K. (Shadia Khan), Karmaus, W. J. (Wilfried J.J.), Jiang, Y. (Yu), Erhart, G. (Gertraud), Kronenberg, F. (Florian), Arathimos, R. (Ryan), Sharp, G. C. (Gemma C.), Henderson, A. J. (Alexander John), Fu, Y. (Yu), Piirilä, P. (Päivi), Pietiläinen, K. H. (Kirsi H.), Ollikainen, M. (Miina), Johansson, A. (Asa), Gyllensten, U. (Ulf), de Vries, M. (Maaike), van der Plaat, D. A. (Diana A.), de Jong, K. (Kim), Boezen, H. M. (H. Marike), Hall, I. P. (Ian P.), Tobin, M. D. (Martin D.), Jarvelin, M.-R. (Marjo-Riitta), Holloway, J. W. (John W.), Jarvis, D. (Deborah), and Probst-Hensch, N. M. (Nicole M.)

Abstract

Previous reports link differential DNA methylation (DNAme) to environmental exposures that are associated with lung function. Direct evidence on lung function DNAme is, however, limited. We undertook an agnostic epigenome-wide association study (EWAS) on pre-bronchodilation lung function and its change in adults. In a discovery–replication EWAS design, DNAme in blood and spirometry were measured twice, 6—15 years apart, in the same participants of three adult population-based discovery cohorts (n=2043). Associated DNAme markers (p<5×10−7) were tested in seven replication cohorts (adult: n=3327; childhood: n=420). Technical bias-adjusted residuals of a regression of the normalised absolute β-values on control probe-derived principle components were regressed on level and change of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and their ratio (FEV1/FVC) in the covariate-adjusted discovery EWAS. Inverse-variance-weighted meta-analyses were performed on results from discovery and replication samples in all participants and never-smokers. EWAS signals were enriched for smoking-related DNAme. We replicated 57 lung function DNAme markers in adult, but not childhood samples, all previously associated with smoking. Markers not previously associated with smoking failed replication. cg05575921 (AHRR (aryl hydrocarbon receptor repressor)) showed the statistically most significant association with cross-sectional lung function (FEV1/FVC: pdiscovery=3.96×10−21 and pcombined=7.22×10−50). A score combining 10 DNAme markers previously reported to mediate the effect of smoking on lung function was associated with lung function (FEV1/FVC: p=2.65×10−20). Our results reveal that lung function-associated methylation signals in adults are predominantly smoking related, and possibly of clinical utility in identifying poor lung function and accelerated decline. Larger studies with more repeat time-points are needed to identify lung function DNAme in never-s

Published
2019

3. Meta-analysis of epigenome-wide association studies in neonates reveals widespread differential DNA methylation associated with birthweight

Author

Kupers, L. K. (Leanne K.), Monnereau, C. (Claire), Sharp, G. C. (Gemma C.), Yousefi, P. (Paul), Salas, L. A. (Lucas A.), Ghantous, A. (Akram), Page, C. M. (Christian M.), Reese, S. E. (Sarah E.), Wilcox, A. J. (Allen J.), Czamara, D. (Darina), Starling, A. P. (Anne P.), Novoloaca, A. (Alexei), Lent, S. (Samantha), Roy, R. (Ritu), Hoyo, C. (Cathrine), Breton, C. V. (Carrie, V), Allard, C. (Catherine), Just, A. C. (Allan C.), Bakulski, K. M. (Kelly M.), Holloway, J. W. (John W.), Everson, T. M. (Todd M.), Xu, C.-J. (Cheng-Jian), Huang, R.-C. (Rae-Chi), van der Plaat, D. A. (Diana A.), Wielscher, M. (Matthias), Merid, S. K. (Simon Kebede), Ullemar, V. (Vilhelmina), Rezwan, F. I. (Faisal, I), Lahti, J. (Jari), van Dongen, J. (Jenny), Langie, S. A. (Sabine A. S.), Richardson, T. G. (Tom G.), Magnus, M. C. (Maria C.), Nohr, E. A. (Ellen A.), Xu, Z. (Zongli), Duijts, L. (Liesbeth), Zhao, S. (Shanshan), Zhang, W. (Weiming), Plusquin, M. (Michelle), DeMeo, D. L. (Dawn L.), Solomon, O. (Olivia), Heimovaara, J. H. (Joosje H.), Jima, D. D. (Dereje D.), Gao, L. (Lu), Bustamante, M. (Mariona), Perron, P. (Patrice), Wright, R. O. (Robert O.), Hertz-Picciotto, I. (Irva), Zhang, H. (Hongmei), Karagas, M. R. (Margaret R.), Gehring, U. (Ulrike), Marsit, C. J. (Carmen J.), Beilin, L. J. (Lawrence J.), Vonk, J. M. (Judith M.), Jarvelin, M.-R. (Marjo-Riitta), Bergstrom, A. (Anna), Ortqvist, A. K. (Anne K.), Ewart, S. (Susan), Villa, P. M. (Pia M.), Moore, S. E. (Sophie E.), Willemsen, G. (Gonneke), Standaert, A. R. (Arnout R. L.), Haberg, S. E. (Siri E.), Sorensen, T. I. (Thorkild I. A.), Taylor, J. A. (Jack A.), Raikkonen, K. (Katri), Yang, I. V. (Ivana, V), Kechris, K. (Katerina), Nawrot, T. S. (Tim S.), Silver, M. J. (Matt J.), Gong, Y. Y. (Yun Yun), Richiardi, L. (Lorenzo), Kogevinas, M. (Manolis), Litonjua, A. A. (Augusto A.), Eskenazi, B. (Brenda), Huen, K. (Karen), Mbarek, H. (Hamdi), Maguire, R. L. (Rachel L.), Dwyer, T. (Terence), Vrijheid, M. (Martine), Bouchard, L. (Luigi), Baccarelli, A. A. (Andrea A.), Croen, L. A. (Lisa A.), Karmaus, W. (Wilfried), Anderson, D. (Denise), de Vries, M. (Maaike), Sebert, S. (Sylvain), Kere, J. (Juha), Karlsson, R. (Robert), Arshad, S. H. (Syed Hasan), Hamalainen, E. (Esa), Routledge, M. N. (Michael N.), Boomsma, D. I. (Dorret, I), Feinberg, A. P. (Andrew P.), Newschaffer, C. J. (Craig J.), Govarts, E. (Eva), Moisse, M. (Matthieu), Fallin, M. D. (M. Daniele), Melen, E. (Erik), Prentice, A. M. (Andrew M.), Kajantie, E. (Eero), Almqvist, C. (Catarina), Oken, E. (Emily), Dabelea, D. (Dana), Boezen, H. M. (H. Marike), Melton, P. E. (Phillip E.), Wright, R. J. (Rosalind J.), Koppelman, G. H. (Gerard H.), Trevisi, L. (Letizia), Hivert, M.-F. (Marie-France), Sunyer, J. (Jordi), Munthe-Kaas, M. C. (Monica C.), Murphy, S. K. (Susan K.), Corpeleijn, E. (Eva), Wiemels, J. (Joseph), Holland, N. (Nina), Herceg, Z. (Zdenko), Binder, E. B. (Elisabeth B.), Smith, G. D. (George Davey), Jaddoe, V. W. (Vincent W. V.), Lie, R. T. (Rolv T.), Nystad, W. (Wenche), London, S. J. (Stephanie J.), Lawlor, D. A. (Debbie A.), Relton, C. L. (Caroline L.), Snieder, H. (Harold), Felix, J. F. (Janine F.), Kupers, L. K. (Leanne K.), Monnereau, C. (Claire), Sharp, G. C. (Gemma C.), Yousefi, P. (Paul), Salas, L. A. (Lucas A.), Ghantous, A. (Akram), Page, C. M. (Christian M.), Reese, S. E. (Sarah E.), Wilcox, A. J. (Allen J.), Czamara, D. (Darina), Starling, A. P. (Anne P.), Novoloaca, A. (Alexei), Lent, S. (Samantha), Roy, R. (Ritu), Hoyo, C. (Cathrine), Breton, C. V. (Carrie, V), Allard, C. (Catherine), Just, A. C. (Allan C.), Bakulski, K. M. (Kelly M.), Holloway, J. W. (John W.), Everson, T. M. (Todd M.), Xu, C.-J. (Cheng-Jian), Huang, R.-C. (Rae-Chi), van der Plaat, D. A. (Diana A.), Wielscher, M. (Matthias), Merid, S. K. (Simon Kebede), Ullemar, V. (Vilhelmina), Rezwan, F. I. (Faisal, I), Lahti, J. (Jari), van Dongen, J. (Jenny), Langie, S. A. (Sabine A. S.), Richardson, T. G. (Tom G.), Magnus, M. C. (Maria C.), Nohr, E. A. (Ellen A.), Xu, Z. (Zongli), Duijts, L. (Liesbeth), Zhao, S. (Shanshan), Zhang, W. (Weiming), Plusquin, M. (Michelle), DeMeo, D. L. (Dawn L.), Solomon, O. (Olivia), Heimovaara, J. H. (Joosje H.), Jima, D. D. (Dereje D.), Gao, L. (Lu), Bustamante, M. (Mariona), Perron, P. (Patrice), Wright, R. O. (Robert O.), Hertz-Picciotto, I. (Irva), Zhang, H. (Hongmei), Karagas, M. R. (Margaret R.), Gehring, U. (Ulrike), Marsit, C. J. (Carmen J.), Beilin, L. J. (Lawrence J.), Vonk, J. M. (Judith M.), Jarvelin, M.-R. (Marjo-Riitta), Bergstrom, A. (Anna), Ortqvist, A. K. (Anne K.), Ewart, S. (Susan), Villa, P. M. (Pia M.), Moore, S. E. (Sophie E.), Willemsen, G. (Gonneke), Standaert, A. R. (Arnout R. L.), Haberg, S. E. (Siri E.), Sorensen, T. I. (Thorkild I. A.), Taylor, J. A. (Jack A.), Raikkonen, K. (Katri), Yang, I. V. (Ivana, V), Kechris, K. (Katerina), Nawrot, T. S. (Tim S.), Silver, M. J. (Matt J.), Gong, Y. Y. (Yun Yun), Richiardi, L. (Lorenzo), Kogevinas, M. (Manolis), Litonjua, A. A. (Augusto A.), Eskenazi, B. (Brenda), Huen, K. (Karen), Mbarek, H. (Hamdi), Maguire, R. L. (Rachel L.), Dwyer, T. (Terence), Vrijheid, M. (Martine), Bouchard, L. (Luigi), Baccarelli, A. A. (Andrea A.), Croen, L. A. (Lisa A.), Karmaus, W. (Wilfried), Anderson, D. (Denise), de Vries, M. (Maaike), Sebert, S. (Sylvain), Kere, J. (Juha), Karlsson, R. (Robert), Arshad, S. H. (Syed Hasan), Hamalainen, E. (Esa), Routledge, M. N. (Michael N.), Boomsma, D. I. (Dorret, I), Feinberg, A. P. (Andrew P.), Newschaffer, C. J. (Craig J.), Govarts, E. (Eva), Moisse, M. (Matthieu), Fallin, M. D. (M. Daniele), Melen, E. (Erik), Prentice, A. M. (Andrew M.), Kajantie, E. (Eero), Almqvist, C. (Catarina), Oken, E. (Emily), Dabelea, D. (Dana), Boezen, H. M. (H. Marike), Melton, P. E. (Phillip E.), Wright, R. J. (Rosalind J.), Koppelman, G. H. (Gerard H.), Trevisi, L. (Letizia), Hivert, M.-F. (Marie-France), Sunyer, J. (Jordi), Munthe-Kaas, M. C. (Monica C.), Murphy, S. K. (Susan K.), Corpeleijn, E. (Eva), Wiemels, J. (Joseph), Holland, N. (Nina), Herceg, Z. (Zdenko), Binder, E. B. (Elisabeth B.), Smith, G. D. (George Davey), Jaddoe, V. W. (Vincent W. V.), Lie, R. T. (Rolv T.), Nystad, W. (Wenche), London, S. J. (Stephanie J.), Lawlor, D. A. (Debbie A.), Relton, C. L. (Caroline L.), Snieder, H. (Harold), and Felix, J. F. (Janine F.)

Abstract

Birthweight is associated with health outcomes across the life course, DNA methylation may be an underlying mechanism. In this meta-analysis of epigenome-wide association studies of 8,825 neonates from 24 birth cohorts in the Pregnancy And Childhood Epigenetics Consortium, we find that DNA methylation in neonatal blood is associated with birthweight at 914 sites, with a difference in birthweight ranging from −183 to 178 grams per 10% increase in methylation (PBonferroni < 1.06 x 10−7). In additional analyses in 7,278 participants, <1.3% of birthweight-associated differential methylation is also observed in childhood and adolescence, but not adulthood. Birthweight-related CpGs overlap with some Bonferroni-significant CpGs that were previously reported to be related to maternal smoking (55/914, p = 6.12 x 10−74) and BMI in pregnancy (3/914, p = 1.13x10−3), but not with those related to folate levels in pregnancy. Whether the associations that we observe are causal or explained by confounding or fetal growth influencing DNA methylation (i.e. reverse causality) requires further research.

Published
2019

4. Evidence for large-scale gene-by-smoking interaction effects on pulmonary function

Author

Aschard, H. (Hugues), Tobin, M. D. (Martin D), Hancock, D. B. (Dana B), Skurnik, D. (David), Sood, A. (Akshay), James, A. (Alan), Smith, A. V. (Albert Vernon), Manichaikul, A. W. (Ani W), Campbell, A. (Archie), Prins, B. P. (Bram P), Hayward, C. (Caroline), Loth, D. W. (Daan W), Porteous, D. J. (David J), Strachan, D. P. (David P), Zeggini, E. (Eleftheria), O’Connor, G. T. (George T), Brusselle, G. G. (Guy G), Boezen, H. M. (H Marike), Schulz, H. (Holger), Deary, I. J. (Ian J), Hall, I. P. (Ian P), Rudan, I. (Igor), Kaprio, J. (Jaakko), Wilson, J. F. (James F), Wilk, J. B. (Jemma B), Huffman, J. E. (Jennifer E), Zhao, J. H. (Jing Hua), de Jong, K. (Kim), Lyytikäinen, L.-P. (Leo-Pekka), Wain, L. V. (Louise V), Järvelin, M.-R. (Marjo-Riitta), Kähönen, M. (Mika), Fornage, M. (Myriam), Polasek, O. (Ozren), Cassano, P. A. (Patricia A), Barr, R. G. (R Graham), Rawal, R. (Rajesh), Harris, S. E. (Sarah E), Gharib, S. A. (Sina A), Enroth, S. (Stefan), Heckbert, S. R. (Susan R), Lehtimäki, T. (Terho), Gyllensten, U. (Ulf), Understanding Society Scientific Group, Jackson, V. E. (Victoria E), Gudnason, V. (Vilmundur), Tang, W. (Wenbo), Dupuis, J. (Josée), Artigas, M. S. (María Soler), Joshi, A. D. (Amit D), London, S. J. (Stephanie J), Kraft, P. (Peter), Groningen Research Institute for Asthma and COPD (GRIAC), and Life Course Epidemiology (LCE)

Subjects
RISK, Medicin och hälsovetenskap, Science & Technology, PREDICTION, 0104 Statistics, respiratory system, genetic risk score, Medical and Health Sciences, DISEASE, smoking, gene-environment interaction, respiratory tract diseases, LUNG-FUNCTION, OPPORTUNITIES, 1117 Public Health And Health Services, FEV1/FVC, EPIDEMIOLOGY, OBSTRUCTION, GENOME-WIDE ASSOCIATION, ENVIRONMENT INTERACTIONS, gene–environment interaction, Life Sciences & Biomedicine, Public, Environmental & Occupational Health
Abstract

Background: Smoking is the strongest environmental risk factor for reduced pulmonary function. The genetic component of various pulmonary traits has also been demonstrated, and at least 26 loci have been reproducibly associated with either FEV1 (forced expiratory volume in 1 second) or FEV1/FVC (FEV1/forced vital capacity). Although the main effects of smoking and genetic loci are well established, the question of potential gene-by-smoking interaction effect remains unanswered. The aim of the present study was to assess, using a genetic risk score approach, whether the effect of these 26 loci on pulmonary function is influenced by smoking. Methods: We evaluated the interaction between smoking exposure, considered as either ever vs never or pack-years, and a 26-single nucleotide polymorphisms (SNPs) genetic risk score in relation to FEV1 or FEV1/FVC in 50 047 participants of European ancestry from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) and SpiroMeta consortia. Results: We identified an interaction (βint = −0.036, 95% confidence interval, −0.040 to −0.032, P = 0.00057) between an unweighted 26 SNP genetic risk score and smoking status (ever/never) on the FEV1/FVC ratio. In interpreting this interaction, we showed that the genetic risk of falling below the FEV1/FVC threshold used to diagnose chronic obstructive pulmonary disease is higher among ever smokers than among never smokers. A replication analysis in two independent datasets, although not statistically significant, showed a similar trend in the interaction effect. Conclusions: This study highlights the benefit of using genetic risk scores for identifying interactions missed when studying individual SNPs and shows, for the first time, that persons with the highest genetic risk for low FEV1/FVC may be more susceptible to the deleterious effects of smoking.

Published
2017

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