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Your search keyword '"Jordan Rivron"' showing total 2 results
Start Over Author "Jordan Rivron" Topic [sdv.mhep.csc] life sciences [q-bio]/human health and pathology/cardiology and cardiovascular system
2 results on '"Jordan Rivron"'

1. Membrane estrogen receptor alpha (ERα) participates in flow-mediated dilation in a ligand-independent manner

Author

Laurent Loufrani, Marine Adlanmerini, Jean-Marie Foidart, Chanaelle Fébrissy, Julie Favre, Jean-Françoise Arnal, Vincent Procaccio, Rana Zahreddine, Léa Réthoré, Coralyne Proux, Emilie Vessieres, Linda Grimaud, Jordan Rivron, Manuela Cl Garcia, Coralie Fontaine, Gilles Flouriot, Anne-Laure Guihot, Daniel Henrion, Morgane Davezac, Françoise Lenfant, MitoVasc - Physiopathologie Cardiovasculaire et Mitochondriale (MITOVASC), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut des Maladies Métaboliques et Casdiovasculaires (UPS/Inserm U1297 - I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Groupe Interdisciplinaire de Génoprotéomique Appliquée (GIGA-Research), Université de Liège, Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), FRM - DPC20171138957, Fondation pour la Recherche Médicale, Equipe FRM DEQ20160334924, Fondation pour la Recherche Médicale, ANR-18-CE14-0016-01, Agence Nationale de la Recherche, Fondation Lefoulon Delalande, Institut National de la Santé et de la Recherche Médicale, Université de Toulouse, Région Occitanie Pyrénées-Méditerranée, Institut Universitaire de France, ANR-18-CE14-0016,EstroShear,Rôle du récepteur aux œstrogènes alpha dans la mécanotransduction du flux: conséquences physiopathologiques(2018), Henrion, Daniel, APPEL À PROJETS GÉNÉRIQUE 2018 - Rôle du récepteur aux œstrogènes alpha dans la mécanotransduction du flux: conséquences physiopathologiques - - EstroShear2018 - ANR-18-CE14-0016 - AAPG2018 - VALID, Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES), Physiopathologie Cardiovasculaire et Mitochondriale (MITOVASC), Université d'Angers (UA)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), and Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Male, Membrane estrogen receptor, medicine.medical_treatment, [SDV]Life Sciences [q-bio], 030204 cardiovascular system & hematology, Ligands, medicine.disease_cause, Mice, 0302 clinical medicine, cell biology, blood flow, Biology (General), 0303 health sciences, Chemistry, General Neuroscience, resistance arteries, estrogen receptors, General Medicine, [SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Blood Circulation, Medicine, Female, Acetylcholine, Research Article, medicine.drug, Agonist, medicine.medical_specialty, endothelium, medicine.drug_class, QH301-705.5, Science, Alpha (ethology), General Biochemistry, Genetics and Molecular Biology, shear stress, 03 medical and health sciences, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Internal medicine, medicine, Animals, mouse, 030304 developmental biology, General Immunology and Microbiology, Insulin, Estrogen Receptor alpha, Hydrogen Peroxide, Endocrinology, Estrogen receptor alpha, Ex vivo, Oxidative stress
Abstract

Estrogen receptor alpha (ERα) activation by estrogens prevents atheroma through its nuclear action, whereas plasma membrane-located ERα accelerates endothelial healing. The genetic deficiency of ERα was associated with a reduction in flow-mediated dilation (FMD) in one man. Here, we evaluated ex vivo the role of ERα on FMD of resistance arteries. FMD, but not agonist (acetylcholine, insulin)-mediated dilation, was reduced in male and female mice lacking ERα (Esr1-/- mice) compared to wild-type mice and was not dependent on the presence of estrogens. In C451A-ERα mice lacking membrane ERα, not in mice lacking AF2-dependent nuclear ERα actions, FMD was reduced, and restored by antioxidant treatments. Compared to wild-type mice, isolated perfused kidneys of C451A-ERα mice revealed a decreased flow-mediated nitrate production and an increased H2O2 production. Thus, endothelial membrane ERα promotes NO bioavailability through inhibition of oxidative stress and thereby participates in FMD in a ligand-independent manner.

Published
2021

2. Altered Mitochondrial Opa1-Related Fusion in Mouse Promotes Endothelial Cell Dysfunction and Atherosclerosis

Author

Ahmad Chehaitly, Anne-Laure Guihot, Coralyne Proux, Linda Grimaud, Jade Aurrière, Benoit Legouriellec, Jordan Rivron, Emilie Vessieres, Clément Tétaud, Antonio Zorzano, Vincent Procaccio, Françoise Joubaud, Pascal Reynier, Guy Lenaers, Laurent Loufrani, Daniel Henrion, MitoVasc - Physiopathologie Cardiovasculaire et Mitochondriale (MITOVASC), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III [Madrid] (ISC), Institute for Research in Biomedicine [Barcelona, Spain] (IRB), University of Barcelona-Barcelona Institute of Science and Technology (BIST), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), and Henrion, Daniel

Subjects
endocrine system, Artèries, Malalties cardiovasculars, Physiology, Clinical Biochemistry, mitochondrial fusion, blood flow, shear stress, arteries, endothelial cell, atherosclerosis, Arteries, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], Cell Biology, Atherosclerosis, Biochemistry, eye diseases, [SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Cardiovascular diseases, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, [SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], Molecular Biology, Aterosclerosi
Abstract

Flow (shear stress)-mediated dilation (FMD) of resistance arteries is a rapid endothelial response involved in tissue perfusion. FMD is reduced early in cardiovascular diseases, generating a major risk factor for atherosclerosis. As alteration of mitochondrial fusion reduces endothelial cells’ (ECs) sprouting and angiogenesis, we investigated its role in ECs responses to flow. Opa1 silencing reduced ECs (HUVECs) migration and flow-mediated elongation. In isolated perfused resistance arteries, FMD was reduced in Opa1+/− mice, a model of the human disease due to Opa1 haplo-insufficiency, and in mice with an EC specific Opa1 knock-out (EC-Opa1). Reducing mitochondrial oxidative stress restored FMD in EC-Opa1 mice. In isolated perfused kidneys from EC-Opa1 mice, flow induced a greater pressure, less ATP, and more H2O2 production, compared to control mice. Opa1 expression and mitochondrial length were reduced in ECs submitted in vitro to disturbed flow and in vivo in the atheroprone zone of the mouse aortic cross. Aortic lipid deposition was greater in Ldlr−/--Opa1+/- and in Ldlr−/--EC-Opa1 mice than in control mice fed with a high-fat diet. In conclusion, we found that reduction in mitochondrial fusion in mouse ECs altered the dilator response to shear stress due to excessive superoxide production and induced greater atherosclerosis development.

Published
2022

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