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Ischemic preconditioning allows protecting the endothelium against the irreversible injuries like endothelial dysfunctions caused by ischemial/reperfusion episodes. The aim of this study was to develop an in vitro model of hypoxic preconditioning on Human Umbilical Vein Endothelial Cells (HUVEC) to understand the mechanisms of this protection and to investigate the role of some proteins in the protective effects of hypoxia preconditioning. Leucocytes Jurkats adhesion to the endothelial cells was chosen as read-out. Western blot have been realized to analyze the changes in expression of potential interesting proteins.Our results confirm the fundamental role of HSP90 in protecting HIF-1, ERKl/2 and Akt from proteosomal degradation. It also shows that the endothelial dysfunction caused by hypoxia is a consequence of an alteration in eNOS activation by phosphorylation. Finally, this study allows validating the hypothesis of the ER1l/2 participation in HIF-1 activation which expression seems to be reduced by hypoxic preconditioning. However, the preconditioning model used didn’t show a protective effect of preconditioning. Le préconditionnement ischémique permet de protéger l'endothélium contre les effets délétères de l'ischémie/reperfusion et notamment en prévenant les dysfonctions endothéliales.Le but de cette étude était de développer un modèle in vitro de préconditionnement hypoxique sur des cultures de cellules endothéliales issues de cordons ombilicaux humains (HUVEC) afin de comprendre les mécanismes de cette protection et d'investiguer Je rôle de certaines protéines dans la protection offerte par le préconditionnem ent. Le read-out choisi pour la mise au point de ce modèle était l'adhésion de cellules leucocytaires Jurkats sur les HUVECs. Des analyses expressionnelles des protéines d'intérêt ont été réalisées par Western Blot.Nos résultats confirment le rôle fondamental de la protéine HSP90 dans la protection contre la dégradation de HIF-1, ERKl/2 et d'Akt. Ils démontrent également que la dysfonction endothéliale consécutive à l'hypoxie passe par l'altération de l'activation de eNOS via l'inhibition de sa phosphorylation par Akt. Enfin, cette étude permet de valider l'hypothèse de la participation de ERKl/2 dans l'activation de HIF-l a dont l'expression semble diminuée suite au préconditionnement.Le modèle de préconditionnement hypoxique utilisé ne permet cependant pas d'observer un effet protecteur du préconditionnement.

Reperfusion Injury --- Hypoxia, Brain

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Hypoxia, Brain --- Brain Ischemia --- Corpus Striatum --- diagnosis --- metabolism

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Brain damage --- Cerebral ischemia --- Brain Damage, Chronic --- Brain Ischemia --- Hypoxia, Brain --- Prevention --- Congresses --- Congresses --- prevention & control --- therapy --- therapy

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Animals, Newborn --- Cerebrovascular Circulation --- Nitric Oxide --- Hypoxia, Brain --- Pulmonary Wedge Pressure --- Pulmonary Artery --- drug effects --- administration & dosage --- complications --- physiology

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It is well known and researched, that deprivation of oxygen to the brain can quickly result in irreversible damage and death. What is less well known, is that some vertebrate species are exceptionally tolerant of brain hypoxia. The Brain Without Oxygen: Causes of failure - Physiological and molecular mechanisms for survival, Third edition, discusses the mechanisms of brain hypoxia tolerance in these exceptional vertebrates, which include diving marine mammals, high altitude dwellers and the hibernating mammal. Special attention is given to the extraordinary adaptations that allow a few turtle and fish species to tolerate months of brain anoxia. This third, fully updated edition addresses the potential of these animal models as targets for human clinical intervention. Perhaps the most interesting of these, are those involved in the suppression of metabolic activities to new set points well below their normoxic minima or maintenance levels. This volume will be valuable reading for researchers in physiology, medicine and general biological sciences, and of great importance to pharmaceutical companies researching novel models for stroke and brain ischemia.

Cerebral anoxia --- Adaptation (Physiology) --- Brain Diseases --- Central Nervous System --- Central Nervous System Diseases --- Nervous System --- Nervous System Diseases --- Anatomy --- Diseases --- Hypoxia, Brain --- Brain --- Human Anatomy & Physiology --- Health & Biological Sciences --- Neuroscience --- Animal physiology. Animal biophysics --- Neurosciences. --- Animal physiology. --- Animal anatomy. --- Biochemistry. --- Veterinary medicine. --- Animal Physiology. --- Animal Anatomy / Morphology / Histology. --- Biochemistry, general. --- Veterinary Medicine/Veterinary Science. --- Farriery --- Large animal medicine --- Large animal veterinary medicine --- Livestock medicine --- Veterinary science --- Medicine --- Animal health --- Animals --- Domestic animals --- Livestock --- Biological chemistry --- Chemical composition of organisms --- Organisms --- Physiological chemistry --- Biology --- Chemistry --- Medical sciences --- Animal anatomy --- Physiology --- Animal physiology --- Neural sciences --- Neurological sciences --- Nervous system --- Losses --- Composition --- Cerebral anoxia.