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11 results on '"MESH: Endothelium"'

1. Zika virus enhances monocyte adhesion and transmigration favoring viral dissemination to neural cells

Author

Emma Partiot, Nilda Vanesa Ayala-Nunez, Jacky G. Goetz, Gautier Follain, Judith R.E. Roels, Anita Eckly, Béatrice Uring-Lambert, Maxime Chazal, Raphael Gaudin, Gillian Hale, Frank M. J. Jacobs, Sandrine Bourdoulous, Orestis Faklaris, Sherif R. Zaki, Aurélie Hirschler, Nolwenn Jouvenet, Margot Carocci, Florian Bakoa, Sarah Cianférani, Christine Carapito, Frédéric Doussau, Brigid C. Bollweg, François Delalande, Institut de Recherche en Infectiologie de Montpellier (IRIM), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Université de Strasbourg (UNISTRA), Institut National de la Santé et de la Recherche Médicale (INSERM), Immuno-Rhumatologie Moléculaire, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Strasbourg (UNISTRA), Fédération de Médecine Translationnelle de Strasbourg (FMTS), Département Sciences Analytiques et Interactions Ioniques et Biomoléculaires (DSA-IPHC), Institut Pluridisciplinaire Hubert Curien (IPHC), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Centers for Disease Control and Prevention [Atlanta] (CDC), Centers for Disease Control and Prevention, Swammerdam Institute for Life Sciences, University of Amsterdam [Amsterdam] (UvA)-Center for Neurosciences, Génomique virale et vaccination, Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur [Paris], Université Paris Descartes - Paris 5 (UPD5), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), BioCampus Montpellier (BCM), Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Biologie et pharmacologie des plaquettes sanguines: hémostase, thrombose, transfusion, Université de Strasbourg (UNISTRA)-EFS-Institut National de la Santé et de la Recherche Médicale (INSERM), Les Hôpitaux Universitaires de Strasbourg (HUS), Institut des Neurosciences Cellulaires et Intégratives (INCI), Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS), This work has received funding from the French State via the French National Research Agency (ANR) as part of the program Investissements d’avenir (IdEx Université de Strasbourg) to RG. This work was supported by an ATIP-AVENIR starting grant to RG. The research leading to these results has received funding from the People Program (Marie Curie Actions) of the European Union’s Seventh Framework Program (FP7/2007–2013) under REA grant agreement no. PCOFUND-GA-2013-609102, through the PRESTIGE program coordinated by Campus France, and from the French Agency for Research on AIDS and Viral Hepatitis (ANRS), both attributed to NVAN. Experiments conducted by G.F. and J.G.G. were funded by Plan Cancer (OptoMetaTrap), Ligue contre le Cancer, Idex Attractivités (University of Strasbourg), and by institutional funds from INSERM and University of Strasbourg. G.F. was supported by a doctoral fellowship from Ligue Contre le Cancer. Mass spectrometry experiments were supported by the French Proteomic Infrastructure (ProFI, ANR-10-INBS-08-03). F.B. is a recipient of a PhD grant provided by ANRT (Association Nationale de la Recherche et de la Technologie). N.J. is funded by Agence Nationale pour la Recherche (ANR-16-CE15-0025-01), Centre National de la Recherche Scientifique (CNRS), and Institut Pasteur. CDC contributions to this paper written and edited by G.L.H. and B.C.B. in their private capacity. No official support or endorsement by the Centers for Disease Control and Prevention, Department of Health and Human Services is intended, nor should be inferred. All authors read, provided feedback, and approved the paper. The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention. The following reagent was obtained through the NIH AIDS Reagent Program, Division of AIDS, NIAID, NIH: HIV-1 NL4-3 AD8 Infectious Molecular Clone (pNL(AD8)) from Dr. Eric O. Freed (cat# 11346)., ANR-16-CE15-0025,Viro-Storm,Mécanismes de production incontrôlée de cytokines au cours de l'infection virale(2016), European Project: 609102,EC:FP7:PEOPLE,FP7-PEOPLE-2013-COFUND,PRESTIGE(2014), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), BioCampus (BCM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Université de Strasbourg (UNISTRA)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), EFS-Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), jouvenet, nolwenn, Mécanismes de production incontrôlée de cytokines au cours de l'infection virale - - Viro-Storm2016 - ANR-16-CE15-0025 - AAPG2016 - VALID, PRES Towards International Gain of Excellence - PRESTIGE - - EC:FP7:PEOPLE2014-09-01 - 2019-08-31 - 609102 - VALID, Equipe Direction scientifique, Sciences et Technologies de la Musique et du Son (STMS), Université Pierre et Marie Curie - Paris 6 (UPMC)-IRCAM-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-IRCAM-Centre National de la Recherche Scientifique (CNRS), École pratique des hautes études (EPHE), Neuro-Immunologie Virale, Virologie UMR1161 (VIRO), École nationale vétérinaire d'Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA)-Agence nationale de sécurité sanitaire de l'alimentation, de l'environnement et du travail (ANSES), Laboratoire de Photonique Quantique et Moléculaire (LPQM), Centre National de la Recherche Scientifique (CNRS)-CentraleSupélec-École normale supérieure - Cachan (ENS Cachan), Biologie et pharmacologie des plaquettes sanguines: hémostase, thrombose, transfusion (http://www.u949.inserm.fr/), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-EFS, Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Spectrométrie de Masse BioOrganique, Département des Sciences Analytiques, Institut Pluridisciplinaire Hubert Curien, Strasbourg, France (LSMBO-DSA-IPHC), Centre National de la Recherche Scientifique (CNRS), Immunorhumathologie moléculaire, Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), and Molecular Neuroscience (SILS, FNWI)

Subjects
Central Nervous System, 0301 basic medicine, MESH: Neurons, General Physics and Astronomy, MESH: Organoids, MESH: Monocytes, Monocytes, Zika virus, 0302 clinical medicine, MESH: Transendothelial and Transepithelial Migration, Cerebellum, MESH: Animals, lcsh:Science, MESH: Embryonic Stem Cells, ComputingMilieux_MISCELLANEOUS, Zebrafish, [SDV.MP.VIR] Life Sciences [q-bio]/Microbiology and Parasitology/Virology, Neurons, Multidisciplinary, Zika Virus Infection, Cell adhesion molecule, food and beverages, Sciences du Vivant [q-bio]/Microbiologie et Parasitologie, Phenotype, 3. Good health, Cell biology, Organoids, Mechanisms of disease, medicine.anatomical_structure, MESH: Cell Survival, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, Female, Endothelium, Cell Survival, Science, MESH: Zika Virus, Biology, MESH: Endothelium, Article, General Biochemistry, Genetics and Molecular Biology, Virus, MESH: Cell Adhesion, 03 medical and health sciences, Virology, medicine, Animals, Humans, MESH: Central Nervous System, Cellular microbiology, Cell adhesion, MESH: Zebrafish, Embryonic Stem Cells, MESH: Humans, Monocyte, fungi, Transendothelial and Transepithelial Migration, Zika Virus, General Chemistry, biology.organism_classification, Embryonic stem cell, MESH: Cerebellum, Disease Models, Animal, 030104 developmental biology, lcsh:Q, MESH: Disease Models, Animal, Cell Adhesion Molecules, MESH: Female, 030217 neurology & neurosurgery
Abstract

Zika virus (ZIKV) invades and persists in the central nervous system (CNS), causing severe neurological diseases. However the virus journey, from the bloodstream to tissues through a mature endothelium, remains unclear. Here, we show that ZIKV-infected monocytes represent suitable carriers for viral dissemination to the CNS using human primary monocytes, cerebral organoids derived from embryonic stem cells, organotypic mouse cerebellar slices, a xenotypic human-zebrafish model, and human fetus brain samples. We find that ZIKV-exposed monocytes exhibit higher expression of adhesion molecules, and higher abilities to attach onto the vessel wall and transmigrate across endothelia. This phenotype is associated to enhanced monocyte-mediated ZIKV dissemination to neural cells. Together, our data show that ZIKV manipulates the monocyte adhesive properties and enhances monocyte transmigration and viral dissemination to neural cells. Monocyte transmigration may represent an important mechanism required for viral tissue invasion and persistence that could be specifically targeted for therapeutic intervention., Zika virus (ZIKV) can infect the central nervous system, but it is not clear how it reaches the brain. Here, Ayala-Nunez et al. show in ex vivo and in vivo models that ZIKV can hitch a ride in monocytes in a Trojan Horse manner to cross the endothelium and disseminate the virus.

Published
2019
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2. The Many Faces of Bacterium-Endothelium Interactions during Systemic Infections

Author

Guillaume Duménil, Dorian Obino, Pathogénèse des Infections vasculaires / Pathogenesis of Vascular Infections, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Pascale Cossart, Craig R. Roy, Philippe Sansonetti, Lassailly-Bondaz, Anne, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Obino, Dorian

Subjects
Microbiology (medical), [SDV.MHEP.AHA] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], Endothelium, Physiology, MESH: Bacterial Infections, Inflammation, Drug resistance, 030204 cardiovascular system & hematology, Biology, MESH: Endothelium, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, Antibiotic resistance, Intensive care, Drug Resistance, Bacterial, MESH: Drug Resistance, Bacterial, Genetics, medicine, [SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], Animals, Humans, MESH: Animals, Organism, 030304 developmental biology, 0303 health sciences, MESH: Humans, General Immunology and Microbiology, Ecology, Bacteria, 030306 microbiology, Neisseria meningitidis, MESH: Host-Pathogen Interactions, Cell Biology, Bacterial Infections, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, 3. Good health, Endothelial stem cell, MESH: Bacteria, Infectious Diseases, medicine.anatomical_structure, Immunology, Host-Pathogen Interactions, cardiovascular system, Endothelium, Vascular, MESH: Endothelium, Vascular, medicine.symptom, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology
Abstract

Voir aussi le même article publié dans le livre : https://onlinelibrary.wiley.com/doi/book/10.1128/9781683670261 ; Dépôt : https://hal-pasteur.archives-ouvertes.fr/pasteur-03116237; International audience; The endothelium is the layer of endothelial cells lining the inner surface of blood vessels, which span the entire body and ensure the distribution of blood throughout the organism. It is estimated that the human body contains a staggering 100,000 km of blood vessels, more than twice the earth’s circumference. Therefore, a bacterium reaching the circulation is engaged in a network of huge proportions. Moreover, a pathogen traveling through the circulatory system does not encounter a homogeneous environment, as an important feature of the vascular network is its diversity. Although endothelial cells are present in all vessels, the organization of the vessel wall, which is formed by three layers—the tunica intima, media, and adventitia (from the vessel lumen outward)—is different among different vessel types and different organs. Vessels can be first differentiated by the complex extracellular matrix layers surrounding them. For instance, elastic arteries such as the aorta are surrounded by 50 elastic layers, providing them with unique mechanical properties. Second, the cellular content is also different according to vessel type; the walls of arteries and veins contain a layer of smooth muscle cells that gives them the capacity to relax or constrict in response to vasoactive molecules. An additional level of complexity in the network stems from the fact that larger vessels, veins or arteries, are themselves vascularized by smaller vessels, the vasa vasorum.

Published
2019
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3. Fonction plaquettaire et altération de l’hémostase après hémorragie sous arachnoïdienne

Author

perez, pauline, Université Paris Descartes - Faculté de Médecine (UPD5 Médecine), Université Paris Descartes - Paris 5 (UPD5), and Anne-Claire Lukaszewicz

Subjects
Inflammation, MESH: Inflammation, MESH: Angioplasty, MESH: Vasospasm, Intracranial, MESH: Subarachnoid Hemorrhage, MESH: Endothelium, Angioplastie, Vasospasme, Hémorragie sous arachnoïdienne, Plaquettes sanguines, Endothélium, Ischémie retardée, MESH: Ischemia, Delayed cerebral ischemia, MESH: Blood Platelets, MESH: Intracranial Hemorrhages, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

Context: vasospasm and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage (aSAH) remain incompletely understood. Platelet activation and alterations in hemostasis might lead to vasospasm and Delayed Cerebral Ischemia (DCI). We investigated platelet function and hemostasis in aSAH patients over time and compared platelet function of patients with and without DCI. We detailed also platelet functions in SAH patients in comparison with the platelet functional profile obtained in patients having an acute inflammation related to orthopedic surgery. Methods : blood samples were studied after aSAH onset (day 5) and then during period at risk of vasospasm (day 10) for the expression of GpIIbIIIa and P-selectin as well as the aggregation rate in the presence of agonists. Endothelium function was evaluated with plasma factor VIII and von Willebrand. Results : 12 high grade aSAH with coiling aneurysm were include and 6 patients in Postop group. aSAH platelets were activated and remained activated over time, especially on the ADP pathway. Plasma factors increased with DCI, demonstrating a propensity towards endothelial activation. Platelets of SAH and Postop patients were similarly activated.Conclusions: aSAH patients showed severe alterations of platelet function and hemostasis that may play a role in the risk of clotting and ischemia. Some of the hemostasis alterations may be potential biomarkers that can be used to detect vasospasm.; Contexte : les mécanismes menant au vasospasme et à l’ischémie retardée après hémorragie sous arachnoïdienne anévrysmale (HSAa) ne sont pas complètement compris. L’activation plaquettaire et l’altération de l’hémostase pourraient être en lien avec le vasospasme et l’ischémie retardée. Nous avons étudié la fonction plaquettaire de patients avec HSAa au cours du temps, selon la présence d’une ischémie retardée puis comparé à des patients ayant une inflammation aigue en lien avec une chirurgie orthopédique. Méthode : les prélèvements sanguins ont été analysés à J5 et durant la période à risque de vasospasme (J10) pour l’expession de GpIIbIIIa et P-selectine, et pour le niveau d’agrégation en présence d’agoniste. La fonction endothéliale était évaluée par dosage des facteurs VIII et von Willebrand. Résultats : 12 HSAa de haut grade avec une prise en charge endovasculaire ont été incluses ainsi que 6 patients dans le groupe de chirurgie orthopédique. Les plaquettes des patients avec HSAa étaient activées et restaient activées au cours du temps, en particulier sur la voie de l’ADP. Les dosages en facteurs VIII et von Willebrand augmentaient avec l’ischémie retardée, démontrant une importante activation endothéliale. L’activation des plaquettes des patients HSAa et du groupe de chirurgie orthopédique était similaire. Conclusion : les plaquettes et l’hémostase primaire des patients HSAa présentent une altération sévère qui pourrait jouer un rôle dans les ischémies chez ces patients. Certains paramètres pourraient être utilisés comme biomarqueurs pour prédire l’ischémie retardée.

Published
2017

4. Hepatic Oval (Stem) Cell Expression of Endothelial Differentiation Gene Receptors for Lysophosphatidic Acid in Mouse Chronic Liver Injury

Author

Jean Sébastien Saulnier-Blache, Yuri Y. Sautin, James M. Crawford, Bryon E. Petersen, Stanislav I. Svetlov, Marda Jorgensen, Department of Pathology, Immunology and Laboratory Medicine, University of North Florida [Jacksonville] (UNF), Biologie de l'adipocyte, physiologie du tissu adipeux et obésités, Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut Louis Bugnard-Hôpital de Rangueil, CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM), Saulnier-Blache, Jean Sébastien, and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut Louis Bugnard-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
MESH: Cell Differentiation, Cell type, medicine.medical_treatment, Blotting, Western, Immunology, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, MESH: Endothelium, Biology, MESH: Research Support, Non-U.S. Gov't, MESH: Lysophospholipids, Mice, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, MESH: Mice, Inbred C57BL, Lysophosphatidic acid, medicine, Animals, MESH: Blotting, Western, MESH: Animals, Endothelium, Progenitor cell, Receptor, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, MESH: Mice, 030304 developmental biology, 0303 health sciences, Cell growth, Growth factor, Cell Differentiation, MESH: Immunohistochemistry, Hematology, MESH: Research Support, U.S. Gov't, P.H.S, Immunohistochemistry, 3. Good health, Cell biology, Mice, Inbred C57BL, medicine.anatomical_structure, Liver, Biochemistry, chemistry, 030220 oncology & carcinogenesis, Hepatocyte, Lysophospholipids, Stem cell, MESH: Liver
Abstract

Growth factor lysophosphatidic acid (LPA) regulates cell proliferation and differentiation and increases motility and survival in several cell types, mostly via G-protein-coupled receptors encoded by endothelial differentiation genes (EDG). We show herein that hepatic oval (stem) cell proliferation, induced by 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) in a mouse model of chronic liver injury, was associated with the expression of LPA1, LPA2, and LPA3 receptor subtypes; only LPA1 receptor protein was detectable in normal liver by western blot. In the injured liver, enhanced LPA1 receptor was identified predominantly in oval cells along the portal tract, proliferating ductular epithelial cells, and small cells, which were located in the nearby parenchyma and formed clusters. Interestingly, the LPA1 receptor was co-expressed in DDC-treated livers with the stem cell antigen SCA-1, suggesting that this receptor may be associated with bone marrow-derived progenitors. All three receptors for LPA were detected mostly in small cells in the vicinity of the portal tract, and co-localized with the A6 antigen, a marker of ductular oval cells. In addition, hepatic levels of endogenous LPA were significantly higher in DDC-fed mice compared to normal animals. We propose that the expression of diverse LPA receptors may be a necessary part of the mechanism responsible for activation of oval cells during liver injury. As a result, LPA and its analogs may represent critical endogenous mediators, which regulate survival, increase motility, and modulate proliferation and differentiation of hepatocyte progenitors in regenerating liver.

Published
2002
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5. ALZHEIMER'S DISEASE AND VASCULAR FACTORS: FACTS AND THEORIES

Author

Pansari, K., Gupta, Anupam, Thomas, P., Indian Institute of Technology Bombay (IIT Bombay), Water Engineering and Management, Centre de Recherches sur les Très Basses Températures (CRTBT), Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique de Grenoble (INPG)-Université Joseph Fourier - Grenoble 1 (UJF), Laboratoire de Neurosciences Fonctionnelles et Pathologies (LNFP), and Université de Lille, Droit et Santé-Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, MESH: Globus Pallidus, MESH: Psychiatry, MESH: Antigens, CD3, MESH: Comorbidity, MESH: Magnetic Resonance Imaging, MESH: Putamen, MESH: Basal Ganglia, MESH: Tourette Syndrome, MESH: Paraproteinemias, MESH: Neural Conduction, Risk Factors, MESH: Risk Factors, MESH: Child, MESH: Microcirculation, MESH: Caudate Nucleus, MESH: Aged, MESH: Polyneuropathies, MESH: Middle Aged, MESH: Vasculitis, General Medicine, MESH: Electrophysiologic Techniques, Cardiac, MESH: Immunoglobulin M, MESH: Review Literature as Topic, MESH: Conflict of Interest, Cardiovascular Diseases, MESH: Paraproteins, MESH: Great Britain, Female, MESH: Cerebrovascular Disorders, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], MESH: Attention Deficit Disorder with Hyperactivity, MESH: Microscopy, Electron, MESH: Endothelium, MESH: Brain, MESH: Mononeuropathies, Alzheimer Disease, Humans, Aged, MESH: Lymphoma, B-Cell, MESH: Adolescent, MESH: Age Factors, MESH: Obsessive-Compulsive Disorder, MESH: Fascia, MESH: Humans, MESH: Cardiovascular Diseases, MESH: Adult, MESH: Male, Cerebrovascular Disorders, MESH: Drug Industry, MESH: Female, MESH: Alzheimer Disease
Abstract

International audience; Although Alzheimer s disease is classified as a neurodegenerative dementia, in Alzheimer s dementia there is increasing evidence of an association with vascular risk factors and vascular pathology. These observations are supported by epidemiological and pathological studies. Vascular factors may play a significant role in the pathogenesis of Alzheimer s dementia. Further research is needed to explore this relationship. Modification of vascular risk factors could make a significant impact towards prevention and treatment of Alzheimer s disease, which is a distressing and prevalent condition in the community. This article considers the relationship of these vascular risk factors and potential mechanisms associated with the aetiopathogenesis of Alzheimer s dementia.

Published
2002
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6. Chronic Meningococcemia Cutaneous Lesions Involve Meningococcal Perivascular Invasion Through the Remodeling of Endothelial Barriers

Author

Marie-Cécile Vacher-Lavenu, Mathieu Coureuil, Hervé Lécuyer, Johan Chanal, Claire Poyart, Xavier Nassif, Muhamed-Kheir Taha, Philippe Morand, Nicolas Dupin, Agnès Carlotti, Alain Schmitt, Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Paris Descartes - Paris 5 (UPD5), CHU Necker - Enfants Malades [AP-HP], Pathogénie des infections systémiques (Inserm U1002), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Infections Bactériennes Invasives, Institut Pasteur [Paris] (IP), This work was supported by Université Paris Descartes, Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de la Recherche Scientifique (CNRS), Institut Pasteur, and Institut Cochin. The laboratory of X. N. is supported by INSERM, Université Paris Descartes, Agence Nationale de la Recherche, and Fondation pour la Recherche Médicale. The laboratory of M. K. T. is supported by Institut Pasteur and the Department of Health., Université Paris Descartes - Paris 5 (UPD5)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris], and CHU Cochin [AP-HP]

Subjects
Microbiology (medical), Pathology, medicine.medical_specialty, MESH: Skin Diseases, Bacterial, Endothelium, endothelium, skin lesion, Bacteremia, MESH: Endothelium, medicine.disease_cause, Meningococcal disease, MESH: Meningococcal Infections, Sepsis, sepsis, 03 medical and health sciences, neisseria meningitidis, In vivo, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Medicine, Compartment (pharmacokinetics), MESH: Bacteremia, 030304 developmental biology, drug administration routes, 0303 health sciences, 030306 microbiology, business.industry, Neisseria meningitidis, MESH: Chronic Disease, Skin Diseases, Bacterial, medicine.disease, Chronic meningococcemia, 3. Good health, Peripheral, Meningococcal Infections, chronic, Infectious Diseases, medicine.anatomical_structure, Chronic Disease, Immunology, meningococcemia, blood capillaries, business, dislocations
Abstract

International audience; Chronic meningococcemia is a form of sepsis with frequent polymorphous skin lesions. Both in vivo and in vitro data suggest that, in these lesions, meningococci gain access from the capillary lumen to the peripheral extravascular compartment, in the absence of vascular dislocation, through a paraendothelial route.

Published
2012
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7. Encapsulated Bacillus anthracis interacts closely with liver endothelium

Author

Grégory Jouvion, Jean-Philippe Corre, Thomas Candela, Pierre L. Goossens, Alejandro Piris-Gimenez, Huot Khun, Toxines et Pathogénie Bactérienne, Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur [Paris], Histotechnologie et Pathologie, Institut Pasteur [Paris], Délégation Générale pour l'Armement grant (no. 04.34.025), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), and Institut Pasteur [Paris] (IP)

Subjects
Bacterial capsule, Bacilli, Phagocytosis, Virulence, Biology, MESH: Virulence, MESH: Endothelium, Microbiology, Anthrax, 03 medical and health sciences, Mice, In vivo, MESH: Bacterial Capsules, MESH: Anthrax, Immunology and Allergy, Animals, MESH: Animals, Endothelium, MESH: Mice, Bacterial Capsules, 030304 developmental biology, 0303 health sciences, Polyglutamate, 030306 microbiology, MESH: Host-Pathogen Interactions, MESH: Polyglutamic Acid, biology.organism_classification, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, 3. Good health, Bacillus anthracis, MESH: Bacillus anthracis, Infectious Diseases, Liver, Polyglutamic Acid, Host-Pathogen Interactions, Female, MESH: Female, Bacteria, MESH: Liver
Abstract

International audience; BACKGROUND: The Bacillus anthracis poly-gamma-D-glutamate capsule is essential for virulence. It impedes phagocytosis and protects bacilli from the immune system, thus promoting systemic dissemination. METHODS: To further define the virulence mechanisms brought into play by the capsule, we characterized the interactions between encapsulated nontoxinogenic B. anthracis and its host in vivo through histological analysis, perfusion, and competition experiments with purified capsule. RESULTS: Clearance of encapsulated bacilli from the blood was rapid (>90% clearance within 5 min), with 75% of the bacteria being trapped in the liver. Competition experiments with purified capsule polyglutamate inhibited this interaction. At the septicemic phase of cutaneous infection with spores, the encapsulated bacilli were trapped in the vascular spaces of the liver and interacted closely with the liver endothelium in the sinusoids and terminal and portal veins. They often grow as microcolonies containing capsular material shed by the bacteria. CONCLUSION: We show that, in addition to its inhibitory effect on the interaction with the immune system, the capsule surrounding B. anthracis plays an active role in mediating the trapping of the bacteria within the liver and may thus contribute to anthrax pathogenesis. Because other microorganisms produce polyglutamate, it may also represent a general mechanism of virulence or in vivo survival.

Published
2009
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8. Platelet microparticles: a new player in malaria parasite cytoadherence to human brain endothelium

Author

Valery Combes, Georges E. Grau, Marie-Christine Alessi, Giovanna Chimini, Dorothée Faille, Thierry Fusai, Albin Fontaine, Irène Juhan-Vague, Andrew J. Mitchell, Department of Pathology, The University of Sydney, Unité de Recherche en Biologie et Epidémiologie Parasitaires, Institut de Médecine Tropicale du Service de Santé des Armées, Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Fibrinolyse et Pathologie Vasculaire, Université de la Méditerranée - Aix-Marseille 2-Institut National de la Santé et de la Recherche Médicale (INSERM), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU)

Subjects
CD31, CD36 Antigens, Erythrocytes, CD36, Biochemistry, 0302 clinical medicine, Platelet, MESH: Animals, Malaria, Falciparum, MESH: Plasmodium falciparum, MESH: Blood Platelets, 0303 health sciences, biology, MESH: Malaria, Falciparum, MESH: Erythrocytes, Brain, 3. Good health, Cell biology, Platelet Endothelial Cell Adhesion Molecule-1, medicine.anatomical_structure, [SDV.IMM]Life Sciences [q-bio]/Immunology, Biotechnology, Blood Platelets, Endothelium, Plasmodium falciparum, Malaria, Cerebral, MESH: Endothelium, Blood–brain barrier, MESH: Cell Adhesion, MESH: Malaria, Cerebral, 03 medical and health sciences, MESH: Brain, Genetics, medicine, Cell Adhesion, Animals, Humans, Cell adhesion, Molecular Biology, Neuroinflammation, 030304 developmental biology, MESH: Humans, MESH: Antigens, CD36, MESH: Antigens, CD31, biology.organism_classification, Immunology, biology.protein, 030217 neurology & neurosurgery
Abstract

International audience; Cerebral malaria (CM) is characterized by accumulation of circulating cells within brain microvessels, among which platelets play an important role. In vitro, platelets modulate the cytoadherence of Plasmodium falciparum-parasitized red blood cells (PRBCs) to brain endothelial cells. Here we show for the first time that platelet microparticles (PMPs) are able to bind to PRBCs, thereby transferring platelet antigens to the PRBC surface. This binding is largely specific to PRBCs, because PMPs show little adherence to normal red blood cells. PMP adherence is also dependent on the P. falciparum erythrocyte membrane protein 1 variant expressed by PRBCs. PMP binding to PRBCs decreases after neutralization of PRBC surface proteins by trypsin or after treatment of PMPs with a mAb to platelet-endothelial cell adhesion molecule-1 (CD31) and glycoprotein IV (CD36). Furthermore, PMP uptake is a dynamic process that can be achieved by human brain endothelial cells (HBECs), inducing changes in the endothelial phenotype. Lastly, PMPs dramatically increase PRBC cytoadherence to HBECs. In conclusion, our study identifies several mechanisms by which PMPs may participate in CM pathogenesis while interacting with both PRBCs and HBECs. PMPs thereby provide a novel target for antagonizing interactions between vascular cells that promote microvascular sludging and blood brain barrier alteration during CM.

Published
2009
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9. Role of inflammatory cytokines in the effect of estradiol on atheroma

Author

Jean-Charles Guéry, Jean-François Arnal, F. Tremollieres, Victorine Douin-Echinard, Bertrand Calippe, Pierre Gourdy, Francis Bayard, Françoise Lenfant, Henrik Laurell, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), IFR 31 Louis Bugnard (IFR 31), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Toulouse [Toulouse]-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Université Fédérale Toulouse Midi-Pyrénées, Centre de Physiopathologie Toulouse Purpan (CPTP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Institut Claude de Préval (ICP)

Subjects
MESH: Interleukin-12, MESH: Interleukin-10, Physiology, medicine.medical_treatment, Prostacyclin, 030204 cardiovascular system & hematology, MESH: Atherosclerosis, Mice, 0302 clinical medicine, Transforming Growth Factor beta, MESH: Animals, 0303 health sciences, MESH: Cytokines, biology, Estradiol, MESH: Hypercholesterolemia, Interleukin-12, 3. Good health, Interleukin-10, medicine.anatomical_structure, Cytokines, Female, MESH: Estradiol, medicine.drug, medicine.medical_specialty, Endothelium, MESH: Interferon Type II, Hypercholesterolemia, MESH: Endothelium, Proinflammatory cytokine, 03 medical and health sciences, Interferon-gamma, In vivo, Physiology (medical), Internal medicine, medicine, Animals, Humans, MESH: Mice, MESH: Transforming Growth Factor beta, 030304 developmental biology, Pharmacology, MESH: Humans, Growth factor, Fatty streak, Transforming growth factor beta, medicine.disease, Atherosclerosis, Atheroma, Endocrinology, MESH: Gene Deletion, biology.protein, MESH: Female, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Gene Deletion
Abstract

International audience; 1. Although hormonal therapy (HT) may increase the risk of coronary heart disease (CHD) and stroke in postmenopausal women, epidemiological studies (protection in premenopausal women) suggest and experimental studies (prevention of fatty streak development in animals) demonstrate a major atheroprotective action of estradiol (E2). The understanding of the deleterious and beneficial effects of oestrogens is thus required. 2. The immuno-inflammatory system plays a key role in the development of fatty streak deposit as well as in the rupture of the atherosclerotic plaque. Although E2 favours an anti-inflammatory effect in vitro (cultured cells), it rather elicits a pro-inflammatory response in vivo involving several subpopulations of the immuno-inflammatory system, which could contribute to plaque destabilization. The functional role of several cytokines was explored in hypercholesterolemic mice. The atheroprotective effect of E2 was fully maintained in mice deficient in interferon-g or interleukin-12, as well as IL-10. In contrast, the protective effect of estradiol was abolished and even reversed in hypercholesterolemic mice given a neutralizing anti-transforming growth factor-b (TGF-b) antibody. Endothelium is another important target for E2, since it not only potentiates endothelial nitric oxide and prostacyclin production, but also controls trafficking of the populations of the immuno-inflammatory system. 3. To conclude, the respective actions of oestrogens on the cell populations involved in the pathophysiology of atherothrombosis may be influenced, among others, by the timing of HT initiation, the status of the vessel wall and, as recently demonstrated the status of the TGF-b pathway.

Published
2008
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10. In vivo electrotransfer of interleukin-10 cDNA prevents endothelial upregulation of activated NF-kappaB and adhesion molecules following an atherogenic diet

Author

Potteaux, Stéphan, Deleuze, Virginie, Merval, Régine, Bureau, Michel, Esposito, Bruno, Scherman, Daniel, Tedgui, Alain, Mallat, Ziad, Centre National de la Recherche Scientifique (CNRS), Centre de Recherche Cardiovasculaire de Lariboisiere, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche de Vitry-Alforville, Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-GenCell SA-Centre National de la Recherche Scientifique (CNRS), Unité de Pharmacologie Chimique et Génétique (UPCG - UMR_S 640/UMR 8151), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Descartes - Paris 5 (UPD5)-Institut des sciences du Médicament -Toxicologie - Chimie - Environnement (IFR71), Institut National de la Santé et de la Recherche Médicale (INSERM)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5)-Institut de Chimie du CNRS (INC), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut des sciences du Médicament -Toxicologie - Chimie - Environnement (IFR71), Institut de Recherche pour le Développement (IRD)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Génétique, Pharmacologie Chimique Et, Université Paris Diderot - Paris 7 (UPD7) - Institut National de la Santé et de la Recherche Médicale (INSERM), Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL (ENSCP) - GenCell SA - Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Université Paris Descartes - Paris 5 (UPD5) - Institut des sciences du Médicament -Toxicologie - Chimie - Environnement (IFR71), and Institut National de la Santé et de la Recherche Médicale (INSERM) - Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL (ENSCP) - Centre National de la Recherche Scientifique (CNRS) - Institut de Recherche pour le Développement (IRD) - Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL (ENSCP) - Centre National de la Recherche Scientifique (CNRS) - Institut de Recherche pour le Développement (IRD) - Université Paris Descartes - Paris 5 (UPD5)

Subjects
MESH: Enzyme Activation, MESH: Interleukin-10, DNA, Complementary, [SDV]Life Sciences [q-bio], MESH: NF-kappa B, Vascular Cell Adhesion Molecule-1, MESH: Gene Transfer Techniques, MESH: Endothelium, MESH: Diet, Atherogenic, Mice, MESH: Mice, Inbred C57BL, MESH: Up-Regulation, Animals, MESH: Animals, MESH: Electroporation, Endothelium, MESH: Mice, MESH: Intercellular Adhesion Molecule-1, MESH: Vascular Cell Adhesion Molecule-1, Gene Transfer Techniques, NF-kappa B, MESH: DNA, Complementary, [SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciences, Sinus of Valsalva, Intercellular Adhesion Molecule-1, Interleukin-10, Up-Regulation, [SDV.SP] Life Sciences [q-bio]/Pharmaceutical sciences, Enzyme Activation, Mice, Inbred C57BL, Electroporation, Diet, Atherogenic, Female, MESH: Female, MESH: Sinus of Valsalva
Abstract

International audience; OBJECTIVES: Interleukin (IL)-10 has anti-atherogenic properties. However, the molecular mechanisms involved in IL-10 protection against atherosclerosis in vivo remain poorly understood. In this study, we examined the effect of IL-10 cDNA in vivo electrotransfer on diet-induced, endothelial activation. METHODS: C57BL/6J mice were fed an atherogenic diet for 10 days. Expression of VCAM-1 and ICAM-1 was examined in the aortic sinus, a region predisposed to atherogenesis in mice, using immunohistochemistry. NF-kappaB activation was examined using a monoclonal antibody that selectively reacts with the activated form of the p65 subunit. RESULTS: We detected a low basal expression of activated NF-kappaB, VCAM-1 and ICAM-1 in the endothelium of the aortic sinus. Endothelial expression of activated NF-kappaB, VCAM-1 and ICAM-1 was markedly increased after 10 days on the atherogenic diet (p < 0.001). In vivo electrotransfer of a murine IL-10-encoding plasmid completely prevented diet-induced endothelial upregulation of activated NF-kappaB, VCAM-1 and ICAM-1 (p < 0.01). CONCLUSION: In vivo electrotransfer of IL-10 cDNA prevents diet-induced endothelial activation. These results suggest that the protective effects of IL-10 may already occur in the very early stages of atherogenesis.

Published
2006

11. Protein kinases and the hypoxia-inducible factor-1, two switches in angiogenesis

Author

Nathalie M. Mazure, Jacques Pouysségur, M. C. Brahimi-Horn, Institut de signalisation, biologie du développement et cancer (ISBDC), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA)

Subjects
Vascular Endothelial Growth Factor A, Angiogenesis, MESH: Cell Hypoxia, Gene Expression, Endothelial Growth Factors, MESH: Vascular Endothelial Growth Factors, Neovascularization, chemistry.chemical_compound, 0302 clinical medicine, MESH: Endothelial Growth Factors, Drug Discovery, Nuclear protein, Lymphokines, 0303 health sciences, Neovascularization, Pathologic, Vascular Endothelial Growth Factors, Kinase, Nuclear Proteins, MESH: Transcription Factors, Cell Hypoxia, 3. Good health, Cell biology, DNA-Binding Proteins, Vascular endothelial growth factor, Vascular endothelial growth factor A, 030220 oncology & carcinogenesis, Intercellular Signaling Peptides and Proteins, Hypoxia-Inducible Factor 1, Mitogen-Activated Protein Kinases, medicine.symptom, MESH: Neovascularization, Physiologic, Transcriptional Activation, MESH: Gene Expression, Neovascularization, Physiologic, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, MESH: Endothelium, MESH: Hypoxia-Inducible Factor 1, alpha Subunit, 03 medical and health sciences, medicine, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Endothelium, MESH: Intercellular Signaling Peptides and Proteins, Transcription factor, 030304 developmental biology, Pharmacology, MESH: Humans, MESH: Lymphokines, MESH: Vascular Endothelial Growth Factor A, Hypoxia-Inducible Factor 1, alpha Subunit, MESH: Mitogen-Activated Protein Kinases, HIF1A, MESH: Hypoxia-Inducible Factor 1, chemistry, MESH: Trans-Activation (Genetics), MESH: Neovascularization, Pathologic, MESH: Nuclear Proteins, MESH: DNA-Binding Proteins, Transcription Factors
Abstract

International audience; In the last few decades it has become clear that detailed understanding of the mechanisms of angiogenesis, a process leading to growth of new blood vessels, should lead to improved treatment of diseases such as ischemic disorders and cancer where neovascularization is impaired or activated, respectively. In this review, we will outline some of our recent findings concerning the regulation of the vascular endothelial growth factor (VEGF), a key player in angiogenesis and one of its transcription factors, the hypoxia-inducible factor-1 (HIF-1) a master gene product driving adaptation to hypoxia. We will discuss the observation that growth factors and oncogenic transformation via the mitogen-activated protein kinases p42/p44 MAPKs not only activate the VEGF promoter through the Sp1/AP-2 transcriptional factor complex but also phosphorylate HIF-1alpha leading in turn to enhance HIF-1 dependent transcriptional activation of VEGF. The stress-activated protein kinases (SAPK) also contribute to angiogenesis by stabilizing VEGF mRNA. Finally, we will present recent advances into oxygen-sensing, in particular the HIF-hydroxylases that govern HIF-1alpha instability (PHD2) or inactivation (FIH-1). The revelation of these oxygen sensors has provided pharmacologists with new molecular targets for the development of novel therapies to control angiogenesis either positively or negatively.

Published
2003

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