PLA2G10 Gene Variants, sPLA2 Activity, and Coronary Heart Disease Risk
| Autor: | Jackie A. Cooper, Holly J. Exeter, Michael V. Holmes, Montse Guardiola, Ziad Mallat, Kay-Tee Khaw, Per Eriksson, Anders Franco-Cereceda, Claire Perret, Sonia-Athina Karabina, Gabrielle Paulsson-Berne, Ferdinand M. van’t Hooft, Jutta Palmen, Philippa J. Talmud, Steve E. Humphries, Lasse Folkersen, Ka Wah Li, S. Matthijs Boekholdt, Ewa Ninio |
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| Přispěvatelé: | University College of London [London] (UCL), Universitat Rovira i Virgili, Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Research Unit on Cardiovascular and Metabolic Diseases (ICAN), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut de Cardiométabolisme et Nutrition = Institute of Cardiometabolism and Nutrition [CHU Pitié Salpêtrière] (IHU ICAN), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Karolinska University Hospital [Stockholm], Karolinska Institutet [Stockholm], University of Cambridge [UK] (CAM), Physiopathologie des maladies génétiques d'expression pédiatrique, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Academic Medical Center - Academisch Medisch Centrum [Amsterdam] (AMC), University of Amsterdam [Amsterdam] (UvA), University of Pennsylvania, This work was funded by the British Heart Foundation RG008/014 (S.E. Humphries and P.J. Talmud), RG/10/001/27643 (Z. Mallat), PG07/133/24260 (S.E. Humphries and P.J. Talmud), FS08/048/25628 (P.J. Talmud), and FS/13/6/29977 and by the Medical Research Council UK (Population Health Scientist Fellowship G0802432: M.V. Holmes). S.E. Humphries and Z. Mallat hold Chairs funded by the British Heart Foundation. The EPIC-Norfolk study is sup-ported by a programme grant from the Medical Research Council UK (G1000143). The Advance Study of Aortic Pathology (ASAP) study was funded by the Swedish Research Unit Council (12660), the Swedish Heart-Lung foundation (20120272), and through a private donation from Fredrik Lundberg., Amsterdam Cardiovascular Sciences, Cardiology, Couvet, Sandrine |
| Rok vydání: | 2014 |
| Předmět: |
Male
MESH: Group X Phospholipases A2 [SDV]Life Sciences [q-bio] Coronary Disease [SDV.GEN] Life Sciences [q-bio]/Genetics MESH: Aged 80 and over MESH: Quantitative Trait Heritable MESH: Risk Factors Risk Factors Medicine genetic polymorphism Prospective Studies Prospective cohort study Genetics (clinical) Genetics MESH: Aged Aged 80 and over MESH: Middle Aged MESH: Polymorphism Single Nucleotide MESH: Follow-Up Studies Middle Aged [SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system [SDV] Life Sciences [q-bio] PLA2G10 Cohort Female Cardiology and Cardiovascular Medicine medicine.medical_specialty Polymorphism Single Nucleotide Quantitative Trait Heritable [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system Meta-Analysis as Topic Internal medicine Group X Phospholipases A2 Humans MESH: Meta-Analysis as Topic Gene Aged [SDV.GEN]Life Sciences [q-bio]/Genetics MESH: Humans business.industry Odds ratio Coronary heart disease Confidence interval MESH: Prospective Studies MESH: Male Observational study MESH: Coronary Disease business Chd risk MESH: Female Follow-Up Studies |
| Zdroj: | Circulation: Cardiovascular Genetics Circulation: Cardiovascular Genetics, 2015, 8 (2), pp.356-362. ⟨10.1161/CIRCGENETICS.114.000633⟩ Circulation. Cardiovascular genetics, 8(2), 356-362. Lippincott Williams and Wilkins |
| ISSN: | 1942-3268 1942-325X |
| DOI: | 10.1161/CIRCGENETICS.114.000633⟩ |
| Popis: | Background— Observational studies report that secretory phospholipase A2 (sPLA2) activity is a marker for coronary heart disease (CHD) risk, and activity measures are thought to represent the composite activity of sPLA2-IIA, -V, and -X. The aim of this study was to use genetic variants of PLA2G10 , encoding sPLA2-X, to investigate the contribution of sPLA2-X to the measure of sPLA2 activity and coronary heart disease (CHD) risk traits and outcome. Methods and Results— Three PLA2G10 tagging single-nucleotide polymorphisms (rs72546339, rs72546340, and rs4003232) and a previously studied PLA2G10 coding single-nucleotide polymorphism rs4003228, R38C, were genotyped in a nested case: control cohort drawn from the prospective EPIC-Norfolk Study (2175 cases and 2175 controls). Meta-analysis of rs4003228 (R38C) and CHD was performed using data from the Northwick Park Heart Study II and 2 published cohorts AtheroGene and SIPLAC, providing in total an additional 1884 cases and 3119 controls. EPIC-Norfolk subjects in the highest tertile of sPLA2 activity were older and had higher inflammatory markers compared with those in the lowest tertile for sPLA2 activity. None of the PLA2G10 tagging single-nucleotide polymorphism nor R38C, a functional variant, were significantly associated with sPLA2 activity, intermediate CHD risk traits, or CHD risk. In meta-analysis, the summary odds ratio for R38C was odds ratio=0.97 (95% confidence interval, 0.77–1.22). Conclusions— PLA2G10 variants are not significantly associated with plasma sPLA2 activity or with CHD risk. |
| Databáze: | OpenAIRE |
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