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7 results on '"MESH : Neovascularization, Physiologic"'

1. Interaction of the coiled‐coil domain with glycosaminoglycans protects angiopoietin‐like 4 from proteolysis and regulates its antiangiogenic activity

Author

Sylvie Ricard-Blum, Clément Faye, Corinne Ardidie-Robouant, Clémence Chomel, Laurent Muller, Stéphane Germain, Aurélie Cazes, A. Barret, Catherine Monnot, Elisa Gomez, Marine Bignon, Pathologie vasculaire et endocrinologie rénale - Chaire de médecine expérimentale (INSERM U36), Collège de France (CdF (institution))-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'anatomo-pathologie [CHU HEGP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Institut de biologie et chimie des protéines [Lyon] (IBCP), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Centre interdisciplinaire de recherche en biologie (CIRB), Labex MemoLife, École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), This work was supported by the European Vascular Genomics Network (http://www.evgn.org) (contract LSHMCT-2003-503254), ANR-06-JCJC-0160,ANGPTL4,Role of ANGPTL4 during development and ischemic heart disease(2006), Pathologie vasculaire et endocrinologie rénale, Collège de France ( CdF ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Experimental Medicine Unit, Collège de France ( CdF ), Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Européen Georges Pompidou [APHP] ( HEGP ), Institut de biologie et chimie des protéines [Lyon] ( IBCP ), Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique ( CNRS ), Service d'hématologie A [CHU HEGP], and ANR-06-JCJC-0160,ANGPTL4,Role of ANGPTL4 during development and ischemic heart disease ( 2006 )

Subjects
MESH : Cell Line, MESH : Angiopoietins, Protein Conformation, Angiogenesis, MESH: Cricetinae, Biochemistry, Extracellular matrix, angiogenesis, MESH: Protein Structure, Tertiary, MESH: Protein Conformation, 0302 clinical medicine, MESH : Lipid Metabolism, Cricetinae, MESH: Animals, MESH : Protein Conformation, Glycosaminoglycans, MESH: Lipid Metabolism, 0303 health sciences, MESH : Neovascularization, Physiologic, medicine.diagnostic_test, Chemistry, MESH : Cricetinae, MESH : Extracellular Matrix, MESH : Protein Binding, MESH: Glycosaminoglycans, [ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, 3. Good health, Cell biology, Endothelial stem cell, 030220 oncology & carcinogenesis, endothelial cell, MESH : Mutation, MESH : Protein Structure, Tertiary, MESH: Neovascularization, Physiologic, Protein Binding, Biotechnology, MESH: Mutation, extracellular matrix, Proteolysis, Neovascularization, Physiologic, Angiopoietin-like 4 Protein, MESH: Extracellular Matrix, Cell Line, Angiopoietin, 03 medical and health sciences, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, MESH : Glycosaminoglycans, Genetics, medicine, Animals, Humans, MESH: Protein Binding, Molecular Biology, 030304 developmental biology, MESH: Humans, hypoxia, MESH : Humans, Lipid Metabolism, Protein Structure, Tertiary, MESH: Cell Line, Cell culture, MESH: Angiopoietins, Mutation, MESH : Animals, Proprotein Convertases, Angiopoietins
Abstract

International audience; Angiopoietin-like 4 (ANGPTL4) is involved in angiogenesis and lipid metabolism. It is secreted by liver and adipose tissues and cleaved to generate circulating coiled-coil domain (CCD) and fibrinogen-like domain (FLD) fragments. The full-length ANGPTL4 produced by hypoxic endothelial cells interacts with the extracellular matrix (ECM). The ECM-bound and soluble forms of ANGPTL4 have antiangiogenic properties. We carried out a structure-function analysis to investigate the regulation of ANGPTL4 bioactivity in endothelial cells. We found that the recombinant CCD binds to the ECM, whereas the FLD is released into the medium. The CCD, like the full-length ANGPTL4, binds to heparan and dermatan sulfates in surface plasmon resonance assays and inhibits endothelial cell adhesion, motility, and tubule-like formation. In endothelial cells, ANGPTL4 is processed in the secretion medium after release from the ECM. This processing is altered by the proprotein convertases inhibitor alpha1-PDX and abolished by the mutation of the (161)RRKR(164) cleavage site without modification of the ECM binding and release. These data suggest that the full-length form, which interacts with heparan sulfate proteoglycans via its CCD, is protected from proteolysis by proprotein convertases and constitutes the major active pool of ANGPTL4 in hypoxic endothelial cells.

Published
2008
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2. Comparative Study of Injury Models for Studying Muscle Regeneration in Mice

Author

Shahragim Tajbakhsh, Cédric Thépenier, David Briand, Aurélie Guguin, Aurore Besnard, Mathilde Latil, Pierre Rocheteau, Grégory Jouvion, Jean-Marc Cavaillon, Quentin Pascal, Fabrice Chrétien, David Hardy, Barbara Gayraud-Morel, Histopathologie humaine et Modèles animaux, Institut Pasteur [Paris], Université Paris Descartes - Paris 5 ( UPD5 ), Institut de Recherche Biomédicale des Armées ( IRBA ), Plateforme de Cytométrie en Flux, GHU A. Chenevier - Henri Mondor ( Inserm U955, équipe 16 ), Cellules Souches et Développement, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique ( CNRS ), Cytokines et Inflammation, This work was financially supported by AFM-vaincre les myopathies ([http://www.afm-telethon.fr/] Role: design, data collection and analysis), Fondation ³Les gueules cassées², Institut Pasteur and Région Ile de France. his work wasalso supported by the agence-nationale-recherche ([http://www.agence-nationale-recherche.fr/], Role:design, data collection and analysis). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of themanuscript, Institut Pasteur [Paris] (IP), Université Paris Descartes - Paris 5 (UPD5), Institut de Recherche Biomédicale des Armées (IRBA), GHU A. Chenevier - Henri Mondor (Inserm U955, équipe 16), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), BENEDIC, Bénédicte, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), and Institut de Recherche Biomédicale des Armées [Brétigny-sur-Orge] (IRBA)

Subjects
Pathology, MESH : Cytokines, Barium Compounds, MESH: Barium Compounds, Pathology and Laboratory Medicine, Muscle Development, MESH : Green Fluorescent Proteins, Mice, Animal Cells, Fibrosis, Freezing, MESH : Chlorides, MESH: Animals, lcsh:Science, MESH : Muscle, Skeletal, Immune Response, Musculoskeletal System, MESH : Macrophages, Innate Immune System, MESH: Cytokines, MESH : Neovascularization, Physiologic, Stem Cells, MESH: Satellite Cells, Skeletal Muscle, MESH : Mice, Transgenic, 3. Good health, [SDV] Life Sciences [q-bio], Neurology, MESH: Cold Injury, Cytokines, Cellular Types, Muscle Regeneration, medicine.medical_specialty, Satellite Cells, Skeletal Muscle, Immune Cells, Immunology, MESH : Muscle Development, Neovascularization, Physiologic, MESH : Myoblasts, Necrosis, 03 medical and health sciences, Signs and Symptoms, Cardiotoxin, MESH: Green Fluorescent Proteins, Regeneration, MESH: Chlorides, Cold Injury, MESH: Elapid Venoms, MESH : Cobra Cardiotoxin Proteins, Blood Cells, MESH: Vascular Endothelial Growth Factor Receptor-2, [ SDV ] Life Sciences [q-bio], [ SDV.BC ] Life Sciences [q-bio]/Cellular Biology, Macrophages, Regeneration (biology), lcsh:R, Biology and Life Sciences, Molecular Development, medicine.disease, Vascular Endothelial Growth Factor Receptor-2, MESH : Necrosis, Mice, Inbred C57BL, Biological Tissue, 030104 developmental biology, Skeletal Muscles, lcsh:Q, Organism Development, Developmental Biology, MESH: Freezing, 0301 basic medicine, Physiology, [SDV]Life Sciences [q-bio], Cobra Cardiotoxin Proteins, Poison control, lcsh:Medicine, Myoblasts, White Blood Cells, Immune Physiology, Neurobiology of Disease and Regeneration, Morphogenesis, Medicine and Health Sciences, Myocyte, MESH: Muscle, Skeletal, Multidisciplinary, Muscles, MESH: Regeneration, MESH: Cobra Cardiotoxin Proteins, medicine.anatomical_structure, MESH: Models, Animal, Models, Animal, MESH: Fibrosis, MESH : Barium Compounds, MESH : Stem Cells, MESH : Fibrosis, MESH: Muscle Development, Basal lamina, Anatomy, Stem cell, medicine.symptom, MESH: Neovascularization, Physiologic, Research Article, MESH : Cold Injury, Histology, MESH: Mice, Transgenic, MESH : Elapid Venoms, Green Fluorescent Proteins, MESH : Vascular Endothelial Growth Factor Receptor-2, Muscle Tissue, Mice, Transgenic, MESH : Regeneration, MESH: Stem Cells, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, MESH : Mice, Inbred C57BL, Biology, Andrology, Chlorides, MESH: Mice, Inbred C57BL, MESH : Satellite Cells, Skeletal Muscle, MESH : Mice, medicine, Animals, MESH: Myoblasts, Muscle, Skeletal, MESH: Mice, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, Inflammation, Elapid Venoms, MESH: Necrosis, MESH: Macrophages, Cell Biology, MESH : Models, Animal, MESH : Freezing, Immune System, MESH : Animals
Abstract

International audience; A longstanding goal in regenerative medicine is to reconstitute functional tissues or organs after injury or disease. Attention has focused on the identification and relative contribution of tissue specific stem cells to the regeneration process. Relatively little is known about how the physiological process is regulated by other tissue constituents. Numerous injury models are used to investigate tissue regeneration, however, these models are often poorly understood. Specifically, for skeletal muscle regeneration several models are reported in the literature, yet the relative impact on muscle physiology and the distinct cells types have not been extensively characterised. We have used transgenic Tg:Pax7nGFP and Flk1GFP/+ mouse models to respectively count the number of muscle stem (satellite) cells (SC) and number/shape of vessels by confocal microscopy. We performed histological and immunostainings to assess the differences in the key regeneration steps. Infiltration of immune cells, chemokines and cytokines production was assessed in vivo by Luminex®.We compared the 4 most commonly used injury models i.e. freeze injury (FI), barium chloride (BaCl2), notexin (NTX) and cardiotoxin (CTX). The FI was the most damaging. In this model, up to 96% of the SCs are destroyed with their surrounding environment (basal lamina and vasculature) leaving a "dead zone" devoid of viable cells. The regeneration process itself is fulfilled in all 4 models with virtually no fibrosis 28 days post-injury, except in the FI model. Inflammatory cells return to basal levels in the CTX, BaCl2 but still significantly high 1-month post-injury in the FI and NTX models. Interestingly the number of SC returned to normal only in the FI, 1-month post-injury, with SCs that are still cycling up to 3-months after the induction of the injury in the other models.We compared the 4 most commonly used injury models i.e. freeze injury (FI), barium chloride (BaCl2), notexin (NTX) and cardiotoxin (CTX). The FI was the most damaging. In this model, up to 96% of the SCs are destroyed with their surrounding environment (basal lamina and vasculature) leaving a "dead zone" devoid of viable cells. The regeneration process itself is fulfilled in all 4 models with virtually no fibrosis 28 days post-injury, except in the FI model. Inflammatory cells return to basal levels in the CTX, BaCl2 but still significantly high 1-month post-injury in the FI and NTX models. Interestingly the number of SC returned to normal only in the FI, 1-month post-injury, with SCs that are still cycling up to 3-months after the induction of the injury in the other models.We compared the 4 most commonly used injury models i.e. freeze injury (FI), barium chloride (BaCl2), notexin (NTX) and cardiotoxin (CTX). The FI was the most damaging. In this model, up to 96% of the SCs are destroyed with their surrounding environment (basal lamina and vasculature) leaving a "dead zone" devoid of viable cells. The regeneration process itself is fulfilled in all 4 models with virtually no fibrosis 28 days post-injury, except in the FI model. Inflammatory cells return to basal levels in the CTX, BaCl2 but still significantly high 1-month post-injury in the FI and NTX models. Interestingly the number of SC returned to normal only in the FI, 1-month post-injury, with SCs that are still cycling up to 3-months after the induction of the injury in the other models.

Published
2016
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3. Widespread lipoplex-mediated gene transfer to vascular endothelial cells and hemangioblasts in the vertebrate embryo

Author

Daniel Scherman, Daisuke Sugiyama, Rodolphe Gautier, Karine Bollerot, Samuel Tozer, Thierry Jaffredo, Virginie Escriou, Laboratoire de Biologie du Développement (LBD), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-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)-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), Laboratoire de Biologie du Développement ( LBD ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Centre National de la Recherche Scientifique ( CNRS ), Unité de Pharmacologie Chimique et Génétique ( UPCG - UMR_S 640/UMR 8151 ), Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL ( ENSCP ) -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 ) -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 ) -Institut de Recherche pour le Développement ( IRD ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), 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), and Génétique, Pharmacologie Chimique Et

Subjects
Vascular Endothelial Growth Factor A, MESH : Va, MESH : Animals, Genetically Modified, MESH: Va, MESH : RNA, Small Interfering, MESH: Hematopoietic Stem Cells, Animals, Genetically Modified, Mice, 0302 clinical medicine, MESH: Genetic Vectors, RNA interference, MESH: RNA, Small Interfering, MESH: Animals, MESH: Endothelial Cells, RNA, Small Interfering, 0303 health sciences, MESH : Neovascularization, Physiologic, Gene Transfer Techniques, Embryo, Transfection, [SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciences, MESH : Mice, Transgenic, MESH : Genetic Vectors, Cell biology, [SDV.SP] Life Sciences [q-bio]/Pharmaceutical sciences, Haematopoiesis, medicine.anatomical_structure, Hemangioblast, MESH: Endothelium, Vascular, Stem cell, Functional genomics, MESH: Neovascularization, Physiologic, Endothelium, MESH: Mice, Transgenic, Genetic Vectors, Neovascularization, Physiologic, Mice, Transgenic, MESH: Gene Transfer Techniques, Biology, MESH: Animals, Genetically Modified, 03 medical and health sciences, MESH : Mice, medicine, Animals, MESH : Gene Transfer Techniques, MESH: Mice, 030304 developmental biology, MESH : Embryo, MESH : Endothelial Cells, MESH : Hematopoietic Stem Cells, MESH: Embryo, Endothelial Cells, Embryo, Mammalian, Hematopoietic Stem Cells, Molecular biology, [ SDV.SP ] Life Sciences [q-bio]/Pharmaceutical sciences, MESH : Endothelium, Vascular, MESH : Liposomes, Liposomes, MESH: Liposomes, Endothelium, Vascular, MESH : Animals, 030217 neurology & neurosurgery, Developmental Biology
Abstract

We report here a method that allows fast, efficient, and low-cost screening for gene function in the vascular system of the vertebrate embryo. Through intracardiac delivery of nucleic acids optimally compacted by a specific cationic lipid, we are able to induce in vivo endothelial cell-specific gain-of-function during development of the vascular network in the chick embryo. When the nucleic acids are delivered during the period of intraembryonic hematopoiesis, aortic hemangioblasts, the forerunners of the hematopoietic stem cells known to derive from the aortic endothelium, are also labeled. Similarly, we show that siRNA could be used to induce loss-of-function in vascular endothelial cells. This gene transfer technique was also applied to the mouse embryo with a high efficiency. The present method allows large-scale analysis and may represent a new and versatile tool for functional genomics.

Published
2006
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4. Inhibition of prolyl hydroxylase domain proteins promotes therapeutic revascularization

Author

Jacques Pouysségur, Amandine Ginouvès, Bernard I. Levy, Micheline Duriez, Jean-Sébastien Silvestre, Edurne Berra, José Vilar, Alice Recalde, Yasmine Zouggari, Céline Loinard, Clément Cochain, Institut de signalisation, biologie du développement et cancer (ISBDC), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Paris-Centre de Recherche Cardiovasculaire (PARCC - UMR-S U970), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Institut de signalisation, biologie du développement et cancer ( ISBDC ), Université Nice Sophia Antipolis ( UNS ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ) -Centre National de la Recherche Scientifique ( CNRS ), Paris-Centre de Recherche Cardiovasculaire ( PARCC - U970 ), Hôpital Européen Georges Pompidou [APHP] ( HEGP ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Laboratoire de génétique et biologie cellulaire ( LGBC ), Université de Versailles Saint-Quentin-en-Yvelines ( UVSQ ) -École pratique des hautes études ( EPHE ) -Centre National de la Recherche Scientifique ( CNRS ), Université Nice Sophia Antipolis (... - 2019) (UNS), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de génétique et biologie cellulaire (LGBC), and Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-École pratique des hautes études (EPHE)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Vascular Endothelial Growth Factor A, MESH: Inflammation, MESH: Signal Transduction, Pathology, MESH : RNA, Messenger, Angiogenesis, Small hairpin RNA, Neovascularization, Mice, 0302 clinical medicine, Ischemia, Medicine, MESH: Animals, MESH: Gene Silencing, [SDV.BDD]Life Sciences [q-bio]/Development Biology, MESH : Macrophages, 0303 health sciences, MESH : Neovascularization, Physiologic, MESH : Procollagen-Proline Dioxygenase, MESH: Hindlimb, MESH: Chemokines, Cell biology, Hindlimb, Femoral Artery, medicine.anatomical_structure, 030220 oncology & carcinogenesis, MESH : Vascular Endothelial Growth Factor A, medicine.symptom, Chemokines, Cardiology and Cardiovascular Medicine, MESH : Gene Therapy, MESH: Neovascularization, Physiologic, MESH: Nitric Oxide Synthase Type III, Plasmids, Signal Transduction, MESH: Femoral Artery, MESH: Procollagen-Proline Dioxygenase, medicine.medical_specialty, MESH : Hypoxia-Inducible Factor 1, alpha Subunit, Nitric Oxide Synthase Type III, Procollagen-Proline Dioxygenase, MESH : Femoral Artery, Neovascularization, Physiologic, MESH : Mice, Inbred C57BL, MESH : Nitric Oxide Synthase Type III, MESH: Hypoxia-Inducible Factor 1, alpha Subunit, Hypoxia-Inducible Factor-Proline Dioxygenases, 03 medical and health sciences, Downregulation and upregulation, MESH : Ischemia, MESH: Mice, Inbred C57BL, MESH: Plasmids, Physiology (medical), MESH : Mice, MESH : Gene Silencing, Gene silencing, Animals, MESH : Chemokines, [ SDV.BDD ] Life Sciences [q-bio]/Development Biology, Gene Silencing, RNA, Messenger, Transcription factor, MESH: Mice, 030304 developmental biology, MESH: RNA, Messenger, MESH : Signal Transduction, Inflammation, Messenger RNA, MESH : Hindlimb, MESH : Inflammation, business.industry, Monocyte, Macrophages, MESH: Vascular Endothelial Growth Factor A, MESH: Macrophages, Genetic Therapy, Hypoxia-Inducible Factor 1, alpha Subunit, Mice, Inbred C57BL, MESH : Plasmids, MESH : Animals, MESH: Gene Therapy, MESH: Ischemia, business
Abstract

Background— The hypoxia-inducible transcription factor (HIF) subunits are destabilized via the O 2 -dependent prolyl hydroxylase domain proteins (PHD1, PHD2, and PHD3). We investigated whether inhibition of PHDs via upregulating HIF might promote postischemic neovascularization. Methods and Results— Mice with right femoral artery ligation were treated, by in vivo electrotransfer, with plasmids encoding for an irrelevant short hairpin RNA (shRNA) (shCON [control]) or specific shRNAs directed against HIF-1α (shHIF-1α), PHD1 (shPHD1), PHD2 (shPHD2), and PHD3 (shPHD3). The silencing of PHDs induced a specific and transient downregulation of their respective mRNA and protein levels at day 2 after ischemia and, as expected, upregulated HIF-1α. As a consequence, 2 key hypoxia-inducible proangiogenic actors, vascular endothelial growth factor-A and endothelial nitric oxide synthase, were upregulated at the mRNA and protein levels. In addition, monocyte chemotactic protein-1 mRNA levels and infiltration of Mac-3-positive macrophages were enhanced in ischemic leg of mice treated with shPHD2 and shPHD3. Furthermore, activation of HIF-1α-related pathways was associated with changes in postischemic neovascularization. At day 14, silencing of PHD2 and PHD3 increased vessel density by 2.2- and 2.6-fold, capillary density by 1.8- and 2.1-fold, and foot perfusion by 1.2- and 1.4-fold, respectively, compared with shCON ( P Conclusions— We demonstrated that a direct inhibition of PHDs, and more particularly PHD3, promoted therapeutic revascularization. Furthermore, we showed that activation of the HIF-1 signaling pathway is required to promote this revascularization.

Published
2009
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5. Microparticles from ischemic muscle promotes postnatal vasculogenesis

Author

Jean-Sébastien Silvestre, José Vilar, Giovanna Chimini, Alain Tedgui, Téni G. Ebrahimian, Aurélie S. Leroyer, Bernard I. Levy, Clément Cochain, Olivier Blanc-Brude, Chantal M. Boulanger, Barend Mees, Alice Recalde, Paris-Centre de Recherche Cardiovasculaire (PARCC - U970), Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Hôpital Européen Georges Pompidou [APHP] (HEGP), Departments of Vascular Surgery and of Cell Biology and Genetics Erasmus, University Medical Center, 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), Paris-Centre de Recherche Cardiovasculaire (PARCC - UMR-S U970), Université Paris Descartes - Paris 5 (UPD5)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Institut National de la Santé et de la Recherche Médicale (INSERM), VU University Medical Center [Amsterdam], Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
MESH: Annexin A5, Angiogenesis, MESH: Membrane Glycoproteins, MESH: Cell Hypoxia, MESH : Reactive Oxygen Species, MESH : Cell-Derived Microparticles, MESH : Membrane Glycoproteins, 030204 cardiovascular system & hematology, MESH: Mice, Knockout, Neovascularization, Mice, 0302 clinical medicine, Annexin, Cell-Derived Microparticles, Ischemia, MESH: Cell-Derived Microparticles, MESH: Animals, MESH: Endothelial Cells, Annexin A5, MESH: NADPH Oxidase, MESH : Ligation, MESH : Muscle, Skeletal, Mice, Knockout, MESH: Muscle, Skeletal, 0303 health sciences, Membrane Glycoproteins, MESH : Neovascularization, Physiologic, Hematopoietic Stem Cell Transplantation, MESH: Reactive Oxygen Species, Cell Differentiation, Cell Hypoxia, Femoral Artery, medicine.anatomical_structure, Enzyme Induction, NADPH Oxidase 2, MESH: ATP-Binding Cassette Transporters, [SDV.IMM]Life Sciences [q-bio]/Immunology, MESH : Cell Hypoxia, MESH: Endothelium, Vascular, medicine.symptom, Cardiology and Cardiovascular Medicine, MESH : Cell Differentiation, MESH: Neovascularization, Physiologic, MESH: Femoral Artery, ATP Binding Cassette Transporter 1, MESH: Cell Differentiation, medicine.medical_specialty, congenital, hereditary, and neonatal diseases and abnormalities, MESH: Enzyme Induction, Endothelium, [SDV.IMM] Life Sciences [q-bio]/Immunology, Neovascularization, Physiologic, MESH : Femoral Artery, 03 medical and health sciences, Vasculogenesis, MESH : NADPH Oxidase, MESH : Ischemia, Physiology (medical), Internal medicine, MESH : Hematopoietic Stem Cell Transplantation, MESH : Mice, medicine, Animals, Humans, MESH : ATP-Binding Cassette Transporters, Progenitor cell, Muscle, Skeletal, MESH: Mice, Ligation, MESH: Hematopoietic Stem Cell Transplantation, 030304 developmental biology, MESH: Humans, business.industry, MESH : Endothelial Cells, MESH : Enzyme Induction, MESH : Humans, Endothelial Cells, NADPH Oxidases, MESH: Ligation, medicine.disease, Transplantation, Endocrinology, MESH : Endothelium, Vascular, Immunology, MESH : Mice, Knockout, ATP-Binding Cassette Transporters, Endothelium, Vascular, MESH : Animals, MESH: Ischemia, business, Reactive Oxygen Species, MESH : Annexin A5
Abstract

Background— We hypothesized that microparticles (MPs) released after ischemia are endogenous signals leading to postischemic vasculogenesis. Methods and Results— MPs from mice ischemic hind-limb muscle were detected by electron microscopy 48 hours after unilateral femoral artery ligation as vesicles of 0.1- to 1-μm diameter. After isolation by sequential centrifugation, flow cytometry analyses showed that the annexin V + MP concentration was 3.5-fold higher in ischemic calves than control muscles (1392±406 versus 394±180 annexin V + MPs per 1 mg; P 144+ ). MPs isolated from ischemic muscles induced more potent in vitro bone marrow–mononuclear cell (BM-MNC) differentiation into cells with endothelial phenotype than those isolated from control muscles. MPs isolated from atherosclerotic plaques were ineffective, whereas those isolated from apoptotic or interleukin-1β–activated endothelial cells also promoted BM-MNC differentiation. Interestingly, MPs from ischemic muscles produced more reactive oxygen species and expressed significantly higher levels of NADPH oxidase p47 (6-fold; P P P Conclusion— MPs produced during tissue ischemia stimulate progenitor cell differentiation and subsequently promote postnatal neovascularization.

Published
2009
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6. Extracellular matrix-bound angiopoietin-like 4 inhibits endothelial cell adhesion, migration, and sprouting and alters actin cytoskeleton

Author

Nicolas Bréchot, Ariane Galaup, Clémence Chomel, Laurent Muller, Marine Bignon, Stéphane Germain, Catherine Monnot, Pierre Corvol, Aurélie Cazes, Holger Weber, Sébastien Le Jan, Pathologie vasculaire et endocrinologie rénale - Chaire de médecine expérimentale (INSERM U36), Collège de France (CdF (institution))-Institut National de la Santé et de la Recherche Médicale (INSERM), Departement of Vascular Biology and Angiogenesis Research, Tumor Biology Center, Centre interdisciplinaire de recherche en biologie (CIRB), Labex MemoLife, École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Mouret, Sandrine, École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Pathologie vasculaire et endocrinologie rénale, Collège de France ( CdF ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Service d'hématologie A [CHU HEGP], and Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Européen Georges Pompidou [APHP] ( HEGP )

Subjects
MESH: Heparin, MESH : Biological Availability, Physiology, Angiogenesis, MESH: Anoxia, MESH : Actins, Extracellular matrix, MESH : Cytoskeleton, Mice, 0302 clinical medicine, Cell Movement, Ischemia, MESH: Blood Proteins, MESH : Cell Movement, MESH: Animals, MESH: Endothelial Cells, Hypoxia, Cytoskeleton, MESH: Cell Movement, Cells, Cultured, MESH: Biological Availability, Tube formation, 0303 health sciences, MESH : Neovascularization, Physiologic, MESH: Hindlimb, MESH : Extracellular Matrix, Blood Proteins, [ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, MESH : Proteoglycans, Extracellular Matrix, Hindlimb, Cell biology, [SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Endothelial stem cell, Biochemistry, 030220 oncology & carcinogenesis, MESH: Proteoglycans, Proteoglycans, Cardiology and Cardiovascular Medicine, MESH: Neovascularization, Physiologic, MESH: Cells, Cultured, MESH : Blood Proteins, MESH : Anoxia, Biological Availability, Neovascularization, Physiologic, MESH : Mice, Inbred C57BL, Angiopoietin-like 4 Protein, In Vitro Techniques, Biology, MESH: Extracellular Matrix, MESH: Actins, Article, MESH: Cell Adhesion, Angiopoietin, 03 medical and health sciences, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, MESH : Ischemia, MESH: Mice, Inbred C57BL, MESH : Mice, MESH : Cells, Cultured, Cell Adhesion, MESH: Cytoskeleton, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Angiopoietin-Like Protein 4, Animals, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, [ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Mice, 030304 developmental biology, MESH : Hindlimb, MESH : Endothelial Cells, Heparin, Endothelial Cells, Actin cytoskeleton, Actins, Mice, Inbred C57BL, MESH : Cell Adhesion, MESH : Heparin, MESH : Animals, MESH: Ischemia, Angiopoietins
Abstract

Angiopoietin-like 4 (ANGPTL4) is a secreted protein that belongs to the angiopoietin family and is involved in angiogenesis and metabolism regulation. We previously reported the induction of angptl4 by hypoxia in endothelial cells and in human ischemic tissues from peripheral artery disease. We here observed in a mouse model of hindlimb ischemia that the mRNA upregulation in the vessels correlates with the accumulation of the full-length protein in ischemic tissues. We then investigated its functions in endothelial cells. In response to hypoxia, endogenous ANGPTL4 accumulates in the subendothelial extracellular matrix (ECM). Although the secreted protein undergoes proteolysis leading to truncated fragments present in the medium, only full-length ANGPTL4 interacts with the ECM. Competition and direct binding assays indicate that the strong interaction of ANGPTL4 with the ECM is heparin/heparan sulfate proteoglycan dependent. The balance between matrix-associated and soluble forms of ANGPTL4 points to the role of the ECM in the regulation of its bioavailability. The angiogenic function of the ECM-bound full-length protein was investigated using either the form associated with the conditioned ECM from ANGPTL4-transfected HEK293 cells or the purified immobilized protein. We show that matrix-associated and immobilized ANGPTL4 limit the formation of actin stress fibers and focal contacts in the adhering endothelial cells and inhibit their adhesion. Immobilized ANGPTL4 also decreases motility of endothelial cells and inhibits the sprouting and tube formation. Altogether, these findings show that hypoxic endothelial cells accumulate ANGPTL4 in the ECM, which in turn negatively regulates their angiogenic capacities through an autocrine pathway.

Published
2006
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7. Angiogenin distribution in human term placenta, and expression by cultured trophoblastic cells

Author

Josette Badet, Danièle Evain-Brion, Yann Bassaglia, Jean-Louis Frendo, Elissavet Hatzi, Nadine Pavlov, Développement humain : Croissance et différenciation, 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)-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)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratory of Biological Chemistry, University of Ioannina, Laboratoire de recherche sur la croissance cellulaire, la réparation et la régénération tissulaires (LRCCRRT), Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-Centre National de la Recherche Scientifique (CNRS), INSERM, Ministère de la Recherche et de la Technologie, Association de la Recherche sur le Cancer, Ligue contre le Cancer, Novo Nordisk Pharmaceutique S.A., 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)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), 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) - Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12) - Centre National de la Recherche Scientifique (CNRS), and Badet, Josette

Subjects
Cancer Research, Physiology, Angiogenesis, MESH: Trophoblasts, MESH : Immunohistochemistry, Placenta, Clinical Biochemistry, MESH: Ribonuclease, Pancreatic, MESH : Ribonuclease, Pancreatic, Gene Expression, MESH : Pregnancy Trimester, Third, MESH : Tissue Distribution, MESH : Fluorescent Antibody Technique, Indirect, chemistry.chemical_compound, 0302 clinical medicine, MESH: Pregnancy, Pregnancy, MESH: Reverse Transcriptase Polymerase Chain Reaction, MESH : Female, Tissue Distribution, Fluorescent Antibody Technique, Indirect, MESH : Culture Media, Conditioned, Tissue homeostasis, reproductive and urinary physiology, Cells, Cultured, In Situ Hybridization, 0303 health sciences, MESH : Neovascularization, Physiologic, MESH: Culture Media, Conditioned, Reverse Transcriptase Polymerase Chain Reaction, MESH : Reverse Transcriptase Polymerase Chain Reaction, Trophoblast, MESH : In Situ Hybridization, MESH: Enzyme-Linked Immunosorbent Assay, MESH: Placenta, MESH : Enzyme-Linked Immunosorbent Assay, Immunohistochemistry, Trophoblasts, Endothelial stem cell, Vascular endothelial growth factor, medicine.anatomical_structure, MESH : Placenta, Placental ribonuclease inhibitor, 030220 oncology & carcinogenesis, embryonic structures, MESH: Pregnancy Trimester, Third, Female, MESH : Trophoblasts, MESH: Neovascularization, Physiologic, MESH: Cells, Cultured, MESH: Gene Expression, Angiogenin, Pregnancy Trimester, Third, Neovascularization, Physiologic, Enzyme-Linked Immunosorbent Assay, Biology, Article, 03 medical and health sciences, Syncytiotrophoblast, MESH: In Situ Hybridization, MESH : Cells, Cultured, medicine, MESH: Fluorescent Antibody Technique, Indirect, Humans, MESH: Tissue Distribution, [SDV.BDLR] Life Sciences [q-bio]/Reproductive Biology, 030304 developmental biology, MESH: Humans, MESH : Humans, MESH: Biological Markers, MESH: Immunohistochemistry, [SDV.BDLR]Life Sciences [q-bio]/Reproductive Biology, Ribonuclease, Pancreatic, Molecular biology, MESH : Biological Markers, MESH : Gene Expression, MESH : Pregnancy, chemistry, Culture Media, Conditioned, MESH: Female, Biomarkers
Abstract

International audience; Human angiogenin is a 14-kDa secreted protein with angiogenic and ribonucleolytic activities. Angiogenin is associated with tumour development but is also present in normal biological fluids and tissues. To further address the physiological role of angiogenin, we studied its expression in situ and in vitro, using the human term placenta as a model of physiological angiogenesis. Angiogenin was immunodetected by light and transmission electron microscopy, and its cellular distribution was established by double immunolabelling with cell markers including von Willebrand factor, platelet/endothelial cell adhesion molecule-1 (PECAM-1), CD34, Tie-2, vascular endothelial cadherin (VE-cadherin), vascular endothelial growth factor receptor-2 (VEGF-R2), erythropoeitin receptor (Epo-R), alpha-smooth muscle actin, CD45, cytokeratin 7, and Ki-67. Angiogenin immunoreactivity was detected in villous and extravillous trophoblasts, the trophoblast basement membrane, the endothelial basal lamina, foetal blood vessels, foetal and maternal red blood cells, and amnionic cells. Its expression was confirmed by in situ hybridisation with a digoxygenin-labelled cDNA probe and reverse transcriptase-polymerase chain reaction amplification. Villous cytotrophoblasts, isolated and differentiated in vitro into a functional syncytiotrophoblast, expressed and secreted angiogenin. Given its known biological activities in vitro and its observed pattern of expression, these data suggest that, in human placenta, angiogenin has a role not only in angiogenesis but also in vascular and tissue homeostasis, maternal immune tolerance of the foetus, and host defences.

Published
2004
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