Lymphangiogenesis-independent resolution of experimental edema
Identifieur interne : 005804 ( Main/Exploration ); précédent : 005803; suivant : 005805Lymphangiogenesis-independent resolution of experimental edema
Auteurs : Emily L. Ongstad ; Echoe M. Bouta ; Jaclynn E. Roberts ; Joseph S. Uzarski ; Sara E. Gibbs ; Michael S. Sabel [États-Unis] ; Vincent M. Cimmino [États-Unis] ; Melissa A. Roberts ; Jeremy GoldmanSource :
- American Journal of Physiology - Heart and Circulatory Physiology [ 0363-6135 ] ; 2010.
Descripteurs français
- KwdFr :
- Animaux, Anticorps monoclonaux (administration et posologie), Cicatrisation de plaie, Facteur de croissance endothéliale vasculaire de type C (métabolisme), Facteurs temps, Femelle, Lymphangiogenèse, Lymphe (métabolisme), Lymphoedème (métabolisme), Lymphoedème (physiopathologie), Lymphographie, Macrophages (métabolisme), Modèles animaux de maladie humaine, Néovascularisation physiologique, Récepteur-2 au facteur croissance endothéliale vasculaire (antagonistes et inhibiteurs), Récepteur-2 au facteur croissance endothéliale vasculaire (métabolisme), Récepteur-3 au facteur croissance endothéliale vasculaire (antagonistes et inhibiteurs), Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme), Souris, Souris de lignée BALB C, Souris de lignée C57BL, Transduction du signal, Vaisseaux capillaires (métabolisme), Vaisseaux capillaires (physiopathologie).
- MESH :
- administration et posologie : Anticorps monoclonaux.
- antagonistes et inhibiteurs : Récepteur-2 au facteur croissance endothéliale vasculaire, Récepteur-3 au facteur croissance endothéliale vasculaire.
- métabolisme : Facteur de croissance endothéliale vasculaire de type C, Lymphe, Lymphoedème, Macrophages, Récepteur-2 au facteur croissance endothéliale vasculaire, Récepteur-3 au facteur croissance endothéliale vasculaire, Vaisseaux capillaires.
- physiopathologie : Lymphoedème, Vaisseaux capillaires.
- Animaux, Cicatrisation de plaie, Facteurs temps, Femelle, Lymphangiogenèse, Lymphographie, Modèles animaux de maladie humaine, Néovascularisation physiologique, Souris, Souris de lignée BALB C, Souris de lignée C57BL, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Antibodies, Monoclonal (administration & dosage), Capillaries (metabolism), Capillaries (physiopathology), Disease Models, Animal, Female, Lymph (metabolism), Lymphangiogenesis, Lymphedema (metabolism), Lymphedema (physiopathology), Lymphography, Macrophages (metabolism), Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Neovascularization, Physiologic, Signal Transduction, Time Factors, Vascular Endothelial Growth Factor C (metabolism), Vascular Endothelial Growth Factor Receptor-2 (antagonists & inhibitors), Vascular Endothelial Growth Factor Receptor-2 (metabolism), Vascular Endothelial Growth Factor Receptor-3 (antagonists & inhibitors), Vascular Endothelial Growth Factor Receptor-3 (metabolism), Wound Healing.
- MESH :
- chemical , administration & dosage : Antibodies, Monoclonal.
- chemical , antagonists & inhibitors : Vascular Endothelial Growth Factor Receptor-2, Vascular Endothelial Growth Factor Receptor-3.
- metabolism : Capillaries, Lymph, Lymphedema, Macrophages, Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor Receptor-2, Vascular Endothelial Growth Factor Receptor-3.
- physiopathology : Capillaries, Lymphedema.
- Animals, Disease Models, Animal, Female, Lymphangiogenesis, Lymphography, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Neovascularization, Physiologic, Signal Transduction, Time Factors, Wound Healing.
Abstract
Vascular endothelial growth factor (VEGF)-C is necessary for lymphangiogenesis, and excess VEGF-C has been shown to be ameliorative for edema produced by lymphatic obstruction in experimental models. However, it has recently been shown that edema can resolve in the mouse tail even in the complete absence of capillary lymphangiogenesis when distal lymph fluid crosses the regenerating wound site interstitially. This finding has raised questions about the action of VEGF-C/VEGF receptor (VEGFR) signaling during the resolution of experimental edema. Here, the roles of VEGFR-2 and VEGFR-3 signaling in edema resolution were explored. It was found that edema resolved following neutralization of either VEGFR-2 or VEGFR-3 in the mouse tail skin, which inhibited lymphangiogenesis. Neutralization of either VEGFR-2 or VEGFR-3 reduced angiogenesis at the site of obstruction at
Url:
DOI: 10.1152/ajpheart.00008.2010
PubMed: 20207821
PubMed Central: 2904140
Affiliations:
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Le document en format XML
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Ongstad</name><affiliation><nlm:aff wicri:cut="; and" id="aff1">Biomedical Engineering Department, Michigan Technological University, Houghton</nlm:aff><wicri:noCountry code="subfield">Houghton</wicri:noCountry></affiliation></author><author><name sortKey="Bouta, Echoe M" sort="Bouta, Echoe M" uniqKey="Bouta E" first="Echoe M." last="Bouta">Echoe M. Bouta</name><affiliation><nlm:aff wicri:cut="; and" id="aff1">Biomedical Engineering Department, Michigan Technological University, Houghton</nlm:aff><wicri:noCountry code="subfield">Houghton</wicri:noCountry></affiliation></author><author><name sortKey="Roberts, Jaclynn E" sort="Roberts, Jaclynn E" uniqKey="Roberts J" first="Jaclynn E." last="Roberts">Jaclynn E. Roberts</name><affiliation><nlm:aff wicri:cut="; and" id="aff1">Biomedical Engineering Department, Michigan Technological University, Houghton</nlm:aff><wicri:noCountry code="subfield">Houghton</wicri:noCountry></affiliation></author><author><name sortKey="Uzarski, Joseph S" sort="Uzarski, Joseph S" uniqKey="Uzarski J" first="Joseph S." last="Uzarski">Joseph S. Uzarski</name><affiliation><nlm:aff wicri:cut="; and" id="aff1">Biomedical Engineering Department, Michigan Technological University, Houghton</nlm:aff><wicri:noCountry code="subfield">Houghton</wicri:noCountry></affiliation></author><author><name sortKey="Gibbs, Sara E" sort="Gibbs, Sara E" uniqKey="Gibbs S" first="Sara E." last="Gibbs">Sara E. Gibbs</name><affiliation><nlm:aff wicri:cut="; and" id="aff1">Biomedical Engineering Department, Michigan Technological University, Houghton</nlm:aff><wicri:noCountry code="subfield">Houghton</wicri:noCountry></affiliation></author><author><name sortKey="Sabel, Michael S" sort="Sabel, Michael S" uniqKey="Sabel M" first="Michael S." last="Sabel">Michael S. Sabel</name><affiliation wicri:level="2"><nlm:aff id="aff2">Division of Surgical Oncology, University of Michigan Health Systems, Ann Arbor, Michigan</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Michigan</region></placeName><wicri:cityArea>Division of Surgical Oncology, University of Michigan Health Systems, Ann Arbor</wicri:cityArea></affiliation></author><author><name sortKey="Cimmino, Vincent M" sort="Cimmino, Vincent M" uniqKey="Cimmino V" first="Vincent M." last="Cimmino">Vincent M. Cimmino</name><affiliation wicri:level="2"><nlm:aff id="aff2">Division of Surgical Oncology, University of Michigan Health Systems, Ann Arbor, Michigan</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Michigan</region></placeName><wicri:cityArea>Division of Surgical Oncology, University of Michigan Health Systems, Ann Arbor</wicri:cityArea></affiliation></author><author><name sortKey="Roberts, Melissa A" sort="Roberts, Melissa A" uniqKey="Roberts M" first="Melissa A." last="Roberts">Melissa A. Roberts</name><affiliation><nlm:aff wicri:cut="; and" id="aff1">Biomedical Engineering Department, Michigan Technological University, Houghton</nlm:aff><wicri:noCountry code="subfield">Houghton</wicri:noCountry></affiliation></author><author><name sortKey="Goldman, Jeremy" sort="Goldman, Jeremy" uniqKey="Goldman J" first="Jeremy" last="Goldman">Jeremy Goldman</name><affiliation><nlm:aff wicri:cut="; and" id="aff1">Biomedical Engineering Department, Michigan Technological University, Houghton</nlm:aff><wicri:noCountry code="subfield">Houghton</wicri:noCountry></affiliation></author></analytic><series><title level="j">American Journal of Physiology - Heart and Circulatory Physiology</title><idno type="ISSN">0363-6135</idno><idno type="eISSN">1522-1539</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antibodies, Monoclonal (administration & dosage)</term><term>Capillaries (metabolism)</term><term>Capillaries (physiopathology)</term><term>Disease Models, Animal</term><term>Female</term><term>Lymph (metabolism)</term><term>Lymphangiogenesis</term><term>Lymphedema (metabolism)</term><term>Lymphedema (physiopathology)</term><term>Lymphography</term><term>Macrophages (metabolism)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred C57BL</term><term>Neovascularization, Physiologic</term><term>Signal Transduction</term><term>Time Factors</term><term>Vascular Endothelial Growth Factor C (metabolism)</term><term>Vascular Endothelial Growth Factor Receptor-2 (antagonists & inhibitors)</term><term>Vascular Endothelial Growth Factor Receptor-2 (metabolism)</term><term>Vascular Endothelial Growth Factor Receptor-3 (antagonists & inhibitors)</term><term>Vascular Endothelial Growth Factor Receptor-3 (metabolism)</term><term>Wound Healing</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Anticorps monoclonaux (administration et posologie)</term><term>Cicatrisation de plaie</term><term>Facteur de croissance endothéliale vasculaire de type C (métabolisme)</term><term>Facteurs temps</term><term>Femelle</term><term>Lymphangiogenèse</term><term>Lymphe (métabolisme)</term><term>Lymphoedème (métabolisme)</term><term>Lymphoedème (physiopathologie)</term><term>Lymphographie</term><term>Macrophages (métabolisme)</term><term>Modèles animaux de maladie humaine</term><term>Néovascularisation physiologique</term><term>Récepteur-2 au facteur croissance endothéliale vasculaire (antagonistes et inhibiteurs)</term><term>Récepteur-2 au facteur croissance endothéliale vasculaire (métabolisme)</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (antagonistes et inhibiteurs)</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme)</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Souris de lignée C57BL</term><term>Transduction du signal</term><term>Vaisseaux capillaires (métabolisme)</term><term>Vaisseaux capillaires (physiopathologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antibodies, Monoclonal</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Vascular Endothelial Growth Factor Receptor-2</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Anticorps monoclonaux</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Récepteur-2 au facteur croissance endothéliale vasculaire</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Capillaries</term><term>Lymph</term><term>Lymphedema</term><term>Macrophages</term><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factor Receptor-2</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type C</term><term>Lymphe</term><term>Lymphoedème</term><term>Macrophages</term><term>Récepteur-2 au facteur croissance endothéliale vasculaire</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term><term>Vaisseaux capillaires</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Lymphoedème</term><term>Vaisseaux capillaires</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Capillaries</term><term>Lymphedema</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Female</term><term>Lymphangiogenesis</term><term>Lymphography</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred C57BL</term><term>Neovascularization, Physiologic</term><term>Signal Transduction</term><term>Time Factors</term><term>Wound Healing</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cicatrisation de plaie</term><term>Facteurs temps</term><term>Femelle</term><term>Lymphangiogenèse</term><term>Lymphographie</term><term>Modèles animaux de maladie humaine</term><term>Néovascularisation physiologique</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Souris de lignée C57BL</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Vascular endothelial growth factor (VEGF)-C is necessary for lymphangiogenesis, and excess VEGF-C has been shown to be ameliorative for edema produced by lymphatic obstruction in experimental models. However, it has recently been shown that edema can resolve in the mouse tail even in the complete absence of capillary lymphangiogenesis when distal lymph fluid crosses the regenerating wound site interstitially. This finding has raised questions about the action of VEGF-C/VEGF receptor (VEGFR) signaling during the resolution of experimental edema. Here, the roles of VEGFR-2 and VEGFR-3 signaling in edema resolution were explored. It was found that edema resolved following neutralization of either VEGFR-2 or VEGFR-3 in the mouse tail skin, which inhibited lymphangiogenesis. Neutralization of either VEGFR-2 or VEGFR-3 reduced angiogenesis at the site of obstruction at <italic>day 10</italic> (9.2 ± 1.2% and 11.5 ± 1.0% blood capillary coverage, respectively) relative to controls (14.3 ± 1.5% blood capillary coverage). Combined VEGFR-2/-3 neutralization more strongly inhibited angiogenesis (6.9 ± 1.5% blood capillary coverage), leading to a reduced wound repair of the lymphatic obstruction and extended edema in the tail skin. In contrast, improved tissue repair of the obstruction site increased edema resolution. Macrophages in the swollen tissue were excluded as contributing factors in the VEGFR-dependent extended edema. These results support a role for VEGFR-2/-3-combined signaling in the resolution of experimental edema that is lymphangiogenesis independent.</p></div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Michigan</li></region></list><tree><noCountry><name sortKey="Bouta, Echoe M" sort="Bouta, Echoe M" uniqKey="Bouta E" first="Echoe M." last="Bouta">Echoe M. Bouta</name><name sortKey="Gibbs, Sara E" sort="Gibbs, Sara E" uniqKey="Gibbs S" first="Sara E." last="Gibbs">Sara E. Gibbs</name><name sortKey="Goldman, Jeremy" sort="Goldman, Jeremy" uniqKey="Goldman J" first="Jeremy" last="Goldman">Jeremy Goldman</name><name sortKey="Ongstad, Emily L" sort="Ongstad, Emily L" uniqKey="Ongstad E" first="Emily L." last="Ongstad">Emily L. Ongstad</name><name sortKey="Roberts, Jaclynn E" sort="Roberts, Jaclynn E" uniqKey="Roberts J" first="Jaclynn E." last="Roberts">Jaclynn E. Roberts</name><name sortKey="Roberts, Melissa A" sort="Roberts, Melissa A" uniqKey="Roberts M" first="Melissa A." last="Roberts">Melissa A. Roberts</name><name sortKey="Uzarski, Joseph S" sort="Uzarski, Joseph S" uniqKey="Uzarski J" first="Joseph S." last="Uzarski">Joseph S. Uzarski</name></noCountry><country name="États-Unis"><region name="Michigan"><name sortKey="Sabel, Michael S" sort="Sabel, Michael S" uniqKey="Sabel M" first="Michael S." last="Sabel">Michael S. Sabel</name></region><name sortKey="Cimmino, Vincent M" sort="Cimmino, Vincent M" uniqKey="Cimmino V" first="Vincent M." last="Cimmino">Vincent M. Cimmino</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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