Inhibition of lymphangiogenesis with resulting lymphedema in transgenic mice expressing soluble VEGF receptor-3.
Identifieur interne : 009A23 ( Main/Exploration ); précédent : 009A22; suivant : 009A24Inhibition of lymphangiogenesis with resulting lymphedema in transgenic mice expressing soluble VEGF receptor-3.
Auteurs : T. M Kinen [Finlande] ; L. Jussila ; T. Veikkola ; T. Karpanen ; M I Kettunen ; K J Pulkkanen ; R. Kauppinen ; D G Jackson ; H. Kubo ; S. Nishikawa ; S. Yl Herttuala ; Kari Alitalo [Finlande]Source :
- Nature medicine [ 1078-8956 ] ; 2001.
Descripteurs français
- KwdFr :
- Animaux, Facteur de croissance endothéliale vasculaire de type C, Facteur de croissance endothéliale vasculaire de type D, Facteurs de croissance endothéliale (génétique), Facteurs de croissance endothéliale (métabolisme), Humains, Lignée cellulaire, Lymphoedème (anatomopathologie), Noeuds lymphatiques (), Néovascularisation pathologique, Phénotype, Récepteur facteur croissance (génétique), Récepteur facteur croissance (métabolisme), Récepteur-3 au facteur croissance endothéliale vasculaire, Récepteurs à activité tyrosine kinase (génétique), Récepteurs à activité tyrosine kinase (métabolisme), Solubilité, Souris, Souris transgéniques, Transduction du signal.
- MESH :
- anatomopathologie : Lymphoedème.
- génétique : Facteurs de croissance endothéliale, Récepteur facteur croissance, Récepteurs à activité tyrosine kinase.
- métabolisme : Facteurs de croissance endothéliale, Récepteur facteur croissance, Récepteurs à activité tyrosine kinase.
- Animaux, Facteur de croissance endothéliale vasculaire de type C, Facteur de croissance endothéliale vasculaire de type D, Humains, Lignée cellulaire, Noeuds lymphatiques, Néovascularisation pathologique, Phénotype, Récepteur-3 au facteur croissance endothéliale vasculaire, Solubilité, Souris, Souris transgéniques, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Cell Line, Endothelial Growth Factors (genetics), Endothelial Growth Factors (metabolism), Humans, Lymph Nodes (blood supply), Lymphedema (pathology), Mice, Mice, Transgenic, Neovascularization, Pathologic, Phenotype, Receptor Protein-Tyrosine Kinases (genetics), Receptor Protein-Tyrosine Kinases (metabolism), Receptors, Growth Factor (genetics), Receptors, Growth Factor (metabolism), Signal Transduction, Solubility, Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor D, Vascular Endothelial Growth Factor Receptor-3.
- MESH :
- chemical , genetics : Endothelial Growth Factors, Receptor Protein-Tyrosine Kinases, Receptors, Growth Factor.
- chemical , metabolism : Endothelial Growth Factors, Receptor Protein-Tyrosine Kinases, Receptors, Growth Factor.
- blood supply : Lymph Nodes.
- pathology : Lymphedema.
- Animals, Cell Line, Humans, Mice, Mice, Transgenic, Neovascularization, Pathologic, Phenotype, Signal Transduction, Solubility, Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor D, Vascular Endothelial Growth Factor Receptor-3.
Abstract
The lymphatic vasculature transports extravasated tissue fluid, macromolecules and cells back into the blood circulation. Recent reports have focused on the molecular mechanisms regulating the lymphatic vessels. Vascular endothelial growth factor (VEGF)-C and VEGF-D have been shown to stimulate lymphangiogenesis and their receptor, VEGFR-3, has been linked to human hereditary lymphedema. Here we show that a soluble form of VEGFR-3 is a potent inhibitor of VEGF-C/VEGF-D signaling, and when expressed in the skin of transgenic mice, it inhibits fetal lymphangiogenesis and induces a regression of already formed lymphatic vessels, though the blood vasculature remains normal. Transgenic mice develop a lymphedema-like phenotype characterized by swelling of feet, edema and dermal fibrosis. They survive the neonatal period in spite of a virtually complete lack of lymphatic vessels in several tissues, and later show regeneration of the lymphatic vasculature, indicating that induction of lymphatic regeneration may also be possible in humans.
DOI: 10.1038/84651
PubMed: 11175851
Affiliations:
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M Kinen</name><affiliation wicri:level="4"><nlm:affiliation>Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Haartman Institute, University of Helsinki, Helsinki, Finland.</nlm:affiliation><country xml:lang="fr">Finlande</country><wicri:regionArea>Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Haartman Institute, University of Helsinki, Helsinki</wicri:regionArea><orgName type="university">Université d'Helsinki</orgName><placeName><settlement type="city">Helsinki</settlement><region type="région" nuts="2">Uusimaa</region></placeName></affiliation></author><author><name sortKey="Jussila, L" sort="Jussila, L" uniqKey="Jussila L" first="L" last="Jussila">L. Jussila</name></author><author><name sortKey="Veikkola, T" sort="Veikkola, T" uniqKey="Veikkola T" first="T" last="Veikkola">T. Veikkola</name></author><author><name sortKey="Karpanen, T" sort="Karpanen, T" uniqKey="Karpanen T" first="T" last="Karpanen">T. 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M Kinen</name><affiliation wicri:level="4"><nlm:affiliation>Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Haartman Institute, University of Helsinki, Helsinki, Finland.</nlm:affiliation><country xml:lang="fr">Finlande</country><wicri:regionArea>Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Haartman Institute, University of Helsinki, Helsinki</wicri:regionArea><orgName type="university">Université d'Helsinki</orgName><placeName><settlement type="city">Helsinki</settlement><region type="région" nuts="2">Uusimaa</region></placeName></affiliation></author><author><name sortKey="Jussila, L" sort="Jussila, L" uniqKey="Jussila L" first="L" last="Jussila">L. Jussila</name></author><author><name sortKey="Veikkola, T" sort="Veikkola, T" uniqKey="Veikkola T" first="T" last="Veikkola">T. Veikkola</name></author><author><name sortKey="Karpanen, T" sort="Karpanen, T" uniqKey="Karpanen T" first="T" last="Karpanen">T. Karpanen</name></author><author><name sortKey="Kettunen, M I" sort="Kettunen, M I" uniqKey="Kettunen M" first="M I" last="Kettunen">M I Kettunen</name></author><author><name sortKey="Pulkkanen, K J" sort="Pulkkanen, K J" uniqKey="Pulkkanen K" first="K J" last="Pulkkanen">K J Pulkkanen</name></author><author><name sortKey="Kauppinen, R" sort="Kauppinen, R" uniqKey="Kauppinen R" first="R" last="Kauppinen">R. Kauppinen</name></author><author><name sortKey="Jackson, D G" sort="Jackson, D G" uniqKey="Jackson D" first="D G" last="Jackson">D G Jackson</name></author><author><name sortKey="Kubo, H" sort="Kubo, H" uniqKey="Kubo H" first="H" last="Kubo">H. Kubo</name></author><author><name sortKey="Nishikawa, S" sort="Nishikawa, S" uniqKey="Nishikawa S" first="S" last="Nishikawa">S. Nishikawa</name></author><author><name sortKey="Yl Herttuala, S" sort="Yl Herttuala, S" uniqKey="Yl Herttuala S" first="S" last="Yl Herttuala">S. Yl Herttuala</name></author><author><name sortKey="Alitalo, K" sort="Alitalo, K" uniqKey="Alitalo K" first="K" last="Alitalo">Kari Alitalo</name><affiliation><country>Finlande</country><placeName><settlement type="city">Helsinki</settlement><region type="région" nuts="2">Uusimaa</region></placeName><orgName type="university">Université d'Helsinki</orgName></affiliation></author></analytic><series><title level="j">Nature medicine</title><idno type="ISSN">1078-8956</idno><imprint><date when="2001" type="published">2001</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Endothelial Growth Factors (genetics)</term><term>Endothelial Growth Factors (metabolism)</term><term>Humans</term><term>Lymph Nodes (blood supply)</term><term>Lymphedema (pathology)</term><term>Mice</term><term>Mice, Transgenic</term><term>Neovascularization, Pathologic</term><term>Phenotype</term><term>Receptor Protein-Tyrosine Kinases (genetics)</term><term>Receptor Protein-Tyrosine Kinases (metabolism)</term><term>Receptors, Growth Factor (genetics)</term><term>Receptors, Growth Factor (metabolism)</term><term>Signal Transduction</term><term>Solubility</term><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factor D</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Facteur de croissance endothéliale vasculaire de type C</term><term>Facteur de croissance endothéliale vasculaire de type D</term><term>Facteurs de croissance endothéliale (génétique)</term><term>Facteurs de croissance endothéliale (métabolisme)</term><term>Humains</term><term>Lignée cellulaire</term><term>Lymphoedème (anatomopathologie)</term><term>Noeuds lymphatiques ()</term><term>Néovascularisation pathologique</term><term>Phénotype</term><term>Récepteur facteur croissance (génétique)</term><term>Récepteur facteur croissance (métabolisme)</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term><term>Récepteurs à activité tyrosine kinase (génétique)</term><term>Récepteurs à activité tyrosine kinase (métabolisme)</term><term>Solubilité</term><term>Souris</term><term>Souris transgéniques</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Endothelial Growth Factors</term><term>Receptor Protein-Tyrosine Kinases</term><term>Receptors, Growth Factor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Endothelial Growth Factors</term><term>Receptor Protein-Tyrosine Kinases</term><term>Receptors, Growth Factor</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Lymphoedème</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Lymph Nodes</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteurs de croissance endothéliale</term><term>Récepteur facteur croissance</term><term>Récepteurs à activité tyrosine kinase</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs de croissance endothéliale</term><term>Récepteur facteur croissance</term><term>Récepteurs à activité tyrosine kinase</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Humans</term><term>Mice</term><term>Mice, Transgenic</term><term>Neovascularization, Pathologic</term><term>Phenotype</term><term>Signal Transduction</term><term>Solubility</term><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factor D</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Facteur de croissance endothéliale vasculaire de type C</term><term>Facteur de croissance endothéliale vasculaire de type D</term><term>Humains</term><term>Lignée cellulaire</term><term>Noeuds lymphatiques</term><term>Néovascularisation pathologique</term><term>Phénotype</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term><term>Solubilité</term><term>Souris</term><term>Souris transgéniques</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The lymphatic vasculature transports extravasated tissue fluid, macromolecules and cells back into the blood circulation. Recent reports have focused on the molecular mechanisms regulating the lymphatic vessels. Vascular endothelial growth factor (VEGF)-C and VEGF-D have been shown to stimulate lymphangiogenesis and their receptor, VEGFR-3, has been linked to human hereditary lymphedema. Here we show that a soluble form of VEGFR-3 is a potent inhibitor of VEGF-C/VEGF-D signaling, and when expressed in the skin of transgenic mice, it inhibits fetal lymphangiogenesis and induces a regression of already formed lymphatic vessels, though the blood vasculature remains normal. Transgenic mice develop a lymphedema-like phenotype characterized by swelling of feet, edema and dermal fibrosis. They survive the neonatal period in spite of a virtually complete lack of lymphatic vessels in several tissues, and later show regeneration of the lymphatic vasculature, indicating that induction of lymphatic regeneration may also be possible in humans.</div></front></TEI><affiliations><list><country><li>Finlande</li></country><region><li>Uusimaa</li></region><settlement><li>Helsinki</li></settlement><orgName><li>Université d'Helsinki</li></orgName></list><tree><noCountry><name sortKey="Jackson, D G" sort="Jackson, D G" uniqKey="Jackson D" first="D G" last="Jackson">D G Jackson</name><name sortKey="Jussila, L" sort="Jussila, L" uniqKey="Jussila L" first="L" last="Jussila">L. Jussila</name><name sortKey="Karpanen, T" sort="Karpanen, T" uniqKey="Karpanen T" first="T" last="Karpanen">T. Karpanen</name><name sortKey="Kauppinen, R" sort="Kauppinen, R" uniqKey="Kauppinen R" first="R" last="Kauppinen">R. Kauppinen</name><name sortKey="Kettunen, M I" sort="Kettunen, M I" uniqKey="Kettunen M" first="M I" last="Kettunen">M I Kettunen</name><name sortKey="Kubo, H" sort="Kubo, H" uniqKey="Kubo H" first="H" last="Kubo">H. Kubo</name><name sortKey="Nishikawa, S" sort="Nishikawa, S" uniqKey="Nishikawa S" first="S" last="Nishikawa">S. Nishikawa</name><name sortKey="Pulkkanen, K J" sort="Pulkkanen, K J" uniqKey="Pulkkanen K" first="K J" last="Pulkkanen">K J Pulkkanen</name><name sortKey="Veikkola, T" sort="Veikkola, T" uniqKey="Veikkola T" first="T" last="Veikkola">T. Veikkola</name><name sortKey="Yl Herttuala, S" sort="Yl Herttuala, S" uniqKey="Yl Herttuala S" first="S" last="Yl Herttuala">S. Yl Herttuala</name></noCountry><country name="Finlande"><region name="Uusimaa"><name sortKey="M Kinen, T" sort="M Kinen, T" uniqKey="M Kinen T" first="T" last="M Kinen">T. M Kinen</name></region><name sortKey="Alitalo, K" sort="Alitalo, K" uniqKey="Alitalo K" first="K" last="Alitalo">Kari Alitalo</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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