Pathophysiological adaptations of resistance arteries in rat offspring exposed in utero to maternal obesity is associated with sex-specific epigenetic alterations

التفاصيل البيبلوغرافية
العنوان: Pathophysiological adaptations of resistance arteries in rat offspring exposed in utero to maternal obesity is associated with sex-specific epigenetic alterations
المؤلفون: Cyrielle Payen, Abigaëlle Guillot, Lily Paillat, Abel Fothi, Abdallah Dib, Jennifer Bourreau, Françoise Schmitt, Laurent Loufrani, Tamas Aranyi, Daniel Henrion, Mathilde Munier, Céline Fassot
المساهمون: Physiopathologie Cardiovasculaire et Mitochondriale (MITOVASC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA), Institute of Enzymology [Budapest], Research Centre for Natural Sciences, Hungarian Academy of Sciences (MTA)-Hungarian Academy of Sciences (MTA), Hémodynamique, Interaction Fibrose et Invasivité tumorales Hépatiques (HIFIH), Université d'Angers (UA), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), Semmelweis University [Budapest], Cardiovascular Functions In Vitro (CARFI), Reference Center for rare Disease of Thyroid and Hormone Receptors, PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM), Fondation de France, grant N° 00075806 'Influence of maternal obesity on fetal programming of cardiovascular abnormalities'
المصدر: HAL
International Journal of Obesity
International Journal of Obesity, Nature Publishing Group, 2021
مصطلحات موضوعية: Male, Potassium Channels, DNA Methylation, Diet, High-Fat, Matrix Metalloproteinases, vascular function, Epigenesis, Genetic, Rats, maternal obesity, Obesity, Maternal, Rats, Sprague-Dawley, fetal programming, Sex Factors, Pregnancy, sexual dimorphism, Prenatal Exposure Delayed Effects, Animals, Female, Vascular Resistance, Collagen, Endothelium, Vascular, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
الوصف: International audience; Backgroung/ Objectives: maternal obesity impacts vascular functions linked to metabolic disorders in offspring, leading to cardiovascular diseases during adulthood. Even if the relation between prenatal conditioning of cardiovascular diseases by maternal obesity and the vascular function begins to be documented, little is known about resistance arteries. They are of particular interest because of their specific role in the regulation of local blood flow. Then our study aims to determine if maternal obesity can directly program fetal vascular dysfunction of resistance arteries, independently of metabolic disorders.Methods: with a model of rats exposed in utero to mild maternal diet-induced obesity (OMO), we investigated third-order mesenteric arteries of 4-month old rats in absence of metabolic disorders. The methylation profile of these vessels was determined by Reduced Representation Bisulfite Sequencing (RRBS). Vascular structure and reactivity were investigated using histomorphometry analysis and wire-myography. Metabolic function was evaluated by insulin and glucose tolerance tests, plasma lipid profile and adipose tissue analysis.Results: at 4 months of age, small mesenteric arteries of OMO presented specific epigenetic modulations of matrix metalloproteinases (MMPs), collagens, and potassium channels genes in association with an outward remodeling and perturbations in the endothelium-dependent vasodilation pathways (greater contribution of EDHFs pathway in OMO males compared to control rats, and greater implication of PGI2 in OMO females compared to control rats). These vascular modifications were detected in absence of metabolic disorders.Conclusion: our study reports a specific methylation profile of resistance arteries associated to vascular remodeling and vasodilation balance perturbations in offspring exposed in utero to maternal obesity, in absence of metabolic dysfunctions.
تدمد: 0307-0565
URL الوصول: https://explore.openaire.eu/search/publication?articleId=pmid_dedup__::ee9f80f51da4f1d9a571c5bef0051942
https://hal.archives-ouvertes.fr/hal-03164923
رقم الأكسشن: edsair.pmid.dedup....ee9f80f51da4f1d9a571c5bef0051942
قاعدة البيانات: OpenAIRE