Global DNA Methylation of Ischemic Stroke Subtypes
Soriano-Tárraga, Carolina (Institut Hospital del Mar d'Investigacions Mèdiques)
Jimenez-Conde, Jordi (Institut Hospital del Mar d'Investigacions Mèdiques)
Giralt Steinhauer, Eva (Institut Hospital del Mar d'Investigacions Mèdiques)
Mola, Marina (Institut Hospital del Mar d'Investigacions Mèdiques)
Ois, Angel (Institut Hospital del Mar d'Investigacions Mèdiques)
Rodríguez-Campello, Ana (Institut Hospital del Mar d'Investigacions Mèdiques)
Cuadrado-Godia, Elisa (Institut Hospital del Mar d'Investigacions Mèdiques)
Fernandez-Cadenas, Israel (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Carrera, Caty (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Montaner, Joan (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Elosua, Roberto (Institut Hospital del Mar d'Investigacions Mèdiques)
Roquer González, Jaume (Institut Hospital del Mar d'Investigacions Mèdiques)
Universitat Autònoma de Barcelona. Departament de Medicina

Data:	2014
Resum:	Ischemic stroke (IS), a heterogeneous multifactorial disorder, is among the leading causes of mortality and long-term disability in the western world. Epidemiological data provides evidence for a genetic component to the disease, but its epigenetic involvement is still largely unknown. Epigenetic mechanisms, such as DNA methylation, change over time and may be associated with aging processes and with modulation of the risk of various pathologies, such as cardiovascular disease and stroke. We analyzed 2 independent cohorts of IS patients. Global DNA methylation was measured by luminometric methylation assay (LUMA) of DNA blood samples. Univariate and multivariate regression analyses were used to assess the methylation differences between the 3 most common IS subtypes, large-artery atherosclerosis (LAA), small-artery disease (SAD), and cardio-aortic embolism (CE). A total of 485 IS patients from 2 independent hospital cohorts (n = 281 and n = 204) were included, distributed across 3 IS subtypes: LAA (78/281, 59/204), SAD (97/281, 53/204), and CE (106/281, 89/204). In univariate analyses, no statistical differences in LUMA levels were observed between the 3 etiologies in either cohort. Multivariate analysis, adjusted by age, sex, hyperlipidemia, and smoking habit, confirmed the lack of differences in methylation levels between the analyzed IS subtypes in both cohorts. Despite differences in pathogenesis, our results showed no global methylation differences between LAA, SAD, and CE subtypes of IS. Further work is required to establish whether the epigenetic mechanism of methylation might play a role in this complex disease.
Ajuts:	Instituto de Salud Carlos III RD12/0042/0020 Instituto de Salud Carlos III PI10/02064 Instituto de Salud Carlos III PI12/01238 Ministerio de Economía, Industria y Competitividad RD12/0014/0005 Ministerio de Economía, Industria y Competitividad CP12/03298
Drets:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Llengua:	Anglès
Document:	Article ; recerca ; Versió publicada
Publicat a:	PloS one, Vol. 9 (april 2014) , ISSN 1932-6203

DOI: 10.1371/journal.pone.0096543
PMID: 24788121

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