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Placental DNA Methylation Adaptation to Maternal Glycemic Response in Pregnancy.
Cardenas, Andres; Gagné-Ouellet, Valerie; Allard, Catherine; Brisson, Diane; Perron, Patrice; Bouchard, Luigi; Hivert, Marie-France.
Afiliación
  • Cardenas A; Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA.
  • Gagné-Ouellet V; Centre de Recherche du Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Quebec, Canada.
  • Allard C; Centre de Recherche du Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Quebec, Canada.
  • Brisson D; Lipidology Unit, Community Genomic Medicine Centre and ECOGENE-21, Department of Medicine, Université de Montréal, Saguenay, Quebec, Canada.
  • Perron P; Centre de Recherche du Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Quebec, Canada.
  • Bouchard L; Centre de Recherche du Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Quebec, Canada.
  • Hivert MF; Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA mhivert@partners.org.
Diabetes ; 67(8): 1673-1683, 2018 08.
Article en En | MEDLINE | ID: mdl-29752424
Maternal hyperglycemia during pregnancy is associated with excess fetal growth and adverse perinatal and developmental outcomes. Placental epigenetic maladaptation may underlie these associations. We performed an epigenome-wide association study (>850,000 CpG sites) of term placentas and prenatal maternal glycemic response 2-h post oral glucose challenge at 24-30 weeks of gestation among 448 mother-infant pairs. Maternal 2-h glycemia postload was strongly associated with lower DNA methylation of four CpG sites (false discovery rate [FDR] q <0.05) within the phosphodiesterase 4B gene (PDE4B). Additionally, three other individual CpG sites were differentially methylated relative to maternal glucose response within the TNFRSF1B, LDLR, and BLM genes (FDR q <0.05). DNA methylation correlated with expression of its respective genes in placental tissue at three out of four independent identified loci: PDE4B (r = 0.31, P < 0.01), TNFRSF1B (r = -0.24, P = 0.013), and LDLR (r = 0.32, P < 0.001). In an independent replication cohort (N = 65-108 samples), results were consistent in direction but not significantly replicated among tested CpG sites in PDE4B and TNFRSF1B Our study provides evidence that maternal glycemic response during pregnancy is associated with placental DNA methylation of key inflammatory genes whose expression levels are partially under epigenetic control.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Placenta / Resistencia a la Insulina / Receptores de LDL / Metilación de ADN / Epigénesis Genética / Receptores Tipo II del Factor de Necrosis Tumoral / Fosfodiesterasas de Nucleótidos Cíclicos Tipo 4 Tipo de estudio: Etiology_studies / Incidence_studies / Observational_studies / Prognostic_studies / Risk_factors_studies Límite: Adult / Female / Humans / Newborn / Pregnancy Idioma: En Revista: Diabetes Año: 2018 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Placenta / Resistencia a la Insulina / Receptores de LDL / Metilación de ADN / Epigénesis Genética / Receptores Tipo II del Factor de Necrosis Tumoral / Fosfodiesterasas de Nucleótidos Cíclicos Tipo 4 Tipo de estudio: Etiology_studies / Incidence_studies / Observational_studies / Prognostic_studies / Risk_factors_studies Límite: Adult / Female / Humans / Newborn / Pregnancy Idioma: En Revista: Diabetes Año: 2018 Tipo del documento: Article Pais de publicación: Estados Unidos