Transgenic Induction of Vascular Endothelial Growth Factor-C Is Strongly Angiogenic in Mouse Embryos but Leads to Persistent Lymphatic Hyperplasia in Adult Tissues
Identifieur interne : 006883 ( Main/Exploration ); précédent : 006882; suivant : 006884Transgenic Induction of Vascular Endothelial Growth Factor-C Is Strongly Angiogenic in Mouse Embryos but Leads to Persistent Lymphatic Hyperplasia in Adult Tissues
Auteurs : Marja Lohela ; Hanna Heloter ; Paula Haiko ; Daniel J. Dumont ; Kari Alitalo [Finlande]Source :
- The American Journal of Pathology [ 0002-9440 ] ; 2008.
Descripteurs français
- KwdFr :
- Animaux, Antigènes CD31 (métabolisme), Cellules endothéliales (cytologie), Cellules endothéliales (métabolisme), Embryon de mammifère (anatomie et histologie), Embryon de mammifère (physiologie), Facteur de croissance endothéliale vasculaire de type C (génétique), Facteur de croissance endothéliale vasculaire de type C (métabolisme), Femelle, Glycoprotéines (métabolisme), Grossesse, Humains, Hyperplasie (anatomopathologie), Hyperplasie (métabolisme), Lymphangiogenèse (physiologie), Marqueurs biologiques (métabolisme), Néovascularisation physiologique, Récepteur-3 au facteur croissance endothéliale vasculaire (génétique), Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme), Souris, Souris transgéniques, Transgènes, Tyrosine (métabolisme), Vaisseaux lymphatiques (anatomopathologie), Vaisseaux lymphatiques (métabolisme).
- MESH :
- anatomie et histologie : Embryon de mammifère.
- anatomopathologie : Hyperplasie, Vaisseaux lymphatiques.
- cytologie : Cellules endothéliales.
- génétique : Facteur de croissance endothéliale vasculaire de type C, Récepteur-3 au facteur croissance endothéliale vasculaire.
- métabolisme : Antigènes CD31, Cellules endothéliales, Facteur de croissance endothéliale vasculaire de type C, Glycoprotéines, Hyperplasie, Marqueurs biologiques, Récepteur-3 au facteur croissance endothéliale vasculaire, Tyrosine, Vaisseaux lymphatiques.
- physiologie : Embryon de mammifère, Lymphangiogenèse.
- Animaux, Femelle, Grossesse, Humains, Néovascularisation physiologique, Souris, Souris transgéniques, Transgènes.
English descriptors
- KwdEn :
- Animals, Antigens, CD31 (metabolism), Biomarkers (metabolism), Embryo, Mammalian (anatomy & histology), Embryo, Mammalian (physiology), Endothelial Cells (cytology), Endothelial Cells (metabolism), Female, Glycoproteins (metabolism), Humans, Hyperplasia (metabolism), Hyperplasia (pathology), Lymphangiogenesis (physiology), Lymphatic Vessels (metabolism), Lymphatic Vessels (pathology), Mice, Mice, Transgenic, Neovascularization, Physiologic, Pregnancy, Transgenes, Tyrosine (metabolism), Vascular Endothelial Growth Factor C (genetics), Vascular Endothelial Growth Factor C (metabolism), Vascular Endothelial Growth Factor Receptor-3 (genetics), Vascular Endothelial Growth Factor Receptor-3 (metabolism).
- MESH :
- chemical , genetics : Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor Receptor-3.
- chemical , metabolism : Antigens, CD31, Biomarkers, Glycoproteins, Tyrosine, Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor Receptor-3.
- anatomy & histology : Embryo, Mammalian.
- cytology : Endothelial Cells.
- metabolism : Endothelial Cells, Hyperplasia, Lymphatic Vessels.
- pathology : Hyperplasia, Lymphatic Vessels.
- physiology : Embryo, Mammalian, Lymphangiogenesis.
- Animals, Female, Humans, Mice, Mice, Transgenic, Neovascularization, Physiologic, Pregnancy, Transgenes.
Abstract
Vascular endothelial growth factor-C (VEGF-C) is the quintessential lymphangiogenic growth factor that is required for the development of the lymphatic system and is capable of stimulating lymphangiogenesis in adults by activating its receptor, VEGFR-3. Although VEGF-C is a major candidate molecule for the development of prolymphangiogenic therapy for defective lymphatic vessels in lymphedema, the stability of lymph vessels generated by exogenous VEGF-C administration is not currently known. We studied VEGF-C-stimulated lymphangiogenesis in inducible transgenic mouse models in which growth factor expression can be spatially and temporally controlled without side effects, such as inflammation. VEGF-C induction in adult mouse skin for 1 to 2 weeks caused robust lymphatic hyperplasia that persisted for at least 6 months. VEGF-C induced lymphangiogenesis in numerous tissues and organs when expressed in the vascular endothelium in either neonates or adult mice. Very few or no effects were observed in either blood vessels or collecting lymph vessels. Additionally, VEGF-C stimulated lymphangiogenesis in embryos after the onset of lymphatic vessel development. Strikingly, a strong angiogenic effect was observed after VEGF-C induction in vascular endothelium at any point before embryonic day 16.5. Our results indicate that blood vessels can undergo VEGF-C-induced angiogenesis even after down-regulation of VEGFR-3 in embryos; however, transient VEGF-C expression in adults can induce long-lasting lymphatic hyperplasia with no obvious side effects on the blood vasculature.
Url:
DOI: 10.2353/ajpath.2008.080378
PubMed: 18988807
PubMed Central: 2626399
Affiliations:
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Dumont</name><affiliation><nlm:aff id="N0x1d3d440N0x3656d10"></nlm:aff></affiliation></author><author><name sortKey="Alitalo, Kari" sort="Alitalo, Kari" uniqKey="Alitalo K" first="Kari" last="Alitalo">Kari Alitalo</name><affiliation><nlm:aff id="N0x1d3d440N0x3656d10"></nlm:aff><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">The American Journal of Pathology</title><idno type="ISSN">0002-9440</idno><idno type="eISSN">1525-2191</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antigens, CD31 (metabolism)</term><term>Biomarkers (metabolism)</term><term>Embryo, Mammalian (anatomy & histology)</term><term>Embryo, Mammalian (physiology)</term><term>Endothelial Cells (cytology)</term><term>Endothelial Cells (metabolism)</term><term>Female</term><term>Glycoproteins (metabolism)</term><term>Humans</term><term>Hyperplasia (metabolism)</term><term>Hyperplasia (pathology)</term><term>Lymphangiogenesis (physiology)</term><term>Lymphatic Vessels (metabolism)</term><term>Lymphatic Vessels (pathology)</term><term>Mice</term><term>Mice, Transgenic</term><term>Neovascularization, Physiologic</term><term>Pregnancy</term><term>Transgenes</term><term>Tyrosine (metabolism)</term><term>Vascular Endothelial Growth Factor C (genetics)</term><term>Vascular Endothelial Growth Factor C (metabolism)</term><term>Vascular Endothelial Growth Factor Receptor-3 (genetics)</term><term>Vascular Endothelial Growth Factor Receptor-3 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antigènes CD31 (métabolisme)</term><term>Cellules endothéliales (cytologie)</term><term>Cellules endothéliales (métabolisme)</term><term>Embryon de mammifère (anatomie et histologie)</term><term>Embryon de mammifère (physiologie)</term><term>Facteur de croissance endothéliale vasculaire de type C (génétique)</term><term>Facteur de croissance endothéliale vasculaire de type C (métabolisme)</term><term>Femelle</term><term>Glycoprotéines (métabolisme)</term><term>Grossesse</term><term>Humains</term><term>Hyperplasie (anatomopathologie)</term><term>Hyperplasie (métabolisme)</term><term>Lymphangiogenèse (physiologie)</term><term>Marqueurs biologiques (métabolisme)</term><term>Néovascularisation physiologique</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (génétique)</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme)</term><term>Souris</term><term>Souris transgéniques</term><term>Transgènes</term><term>Tyrosine (métabolisme)</term><term>Vaisseaux lymphatiques (anatomopathologie)</term><term>Vaisseaux lymphatiques (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, CD31</term><term>Biomarkers</term><term>Glycoproteins</term><term>Tyrosine</term><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" qualifier="anatomie et histologie" xml:lang="fr"><term>Embryon de mammifère</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Hyperplasie</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="anatomy & histology" xml:lang="en"><term>Embryo, Mammalian</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules endothéliales</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelial Cells</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type C</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term><term>Hyperplasia</term><term>Lymphatic Vessels</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes CD31</term><term>Cellules endothéliales</term><term>Facteur de croissance endothéliale vasculaire de type C</term><term>Glycoprotéines</term><term>Hyperplasie</term><term>Marqueurs biologiques</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term><term>Tyrosine</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Hyperplasia</term><term>Lymphatic Vessels</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Embryon de mammifère</term><term>Lymphangiogenèse</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Embryo, Mammalian</term><term>Lymphangiogenesis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Humans</term><term>Mice</term><term>Mice, Transgenic</term><term>Neovascularization, Physiologic</term><term>Pregnancy</term><term>Transgenes</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Grossesse</term><term>Humains</term><term>Néovascularisation physiologique</term><term>Souris</term><term>Souris transgéniques</term><term>Transgènes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Vascular endothelial growth factor-C (VEGF-C) is the quintessential lymphangiogenic growth factor that is required for the development of the lymphatic system and is capable of stimulating lymphangiogenesis in adults by activating its receptor, VEGFR-3. Although VEGF-C is a major candidate molecule for the development of prolymphangiogenic therapy for defective lymphatic vessels in lymphedema, the stability of lymph vessels generated by exogenous VEGF-C administration is not currently known. We studied VEGF-C-stimulated lymphangiogenesis in inducible transgenic mouse models in which growth factor expression can be spatially and temporally controlled without side effects, such as inflammation. VEGF-C induction in adult mouse skin for 1 to 2 weeks caused robust lymphatic hyperplasia that persisted for at least 6 months. VEGF-C induced lymphangiogenesis in numerous tissues and organs when expressed in the vascular endothelium in either neonates or adult mice. Very few or no effects were observed in either blood vessels or collecting lymph vessels. Additionally, VEGF-C stimulated lymphangiogenesis in embryos after the onset of lymphatic vessel development. Strikingly, a strong angiogenic effect was observed after VEGF-C induction in vascular endothelium at any point before embryonic day 16.5. Our results indicate that blood vessels can undergo VEGF-C-induced angiogenesis even after down-regulation of VEGFR-3 in embryos; however, transient VEGF-C expression in adults can induce long-lasting lymphatic hyperplasia with no obvious side effects on the blood vasculature.</p></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="Dumont, Daniel J" sort="Dumont, Daniel J" uniqKey="Dumont D" first="Daniel J." last="Dumont">Daniel J. Dumont</name><name sortKey="Haiko, Paula" sort="Haiko, Paula" uniqKey="Haiko P" first="Paula" last="Haiko">Paula Haiko</name><name sortKey="Heloter, Hanna" sort="Heloter, Hanna" uniqKey="Heloter H" first="Hanna" last="Heloter">Hanna Heloter</name><name sortKey="Lohela, Marja" sort="Lohela, Marja" uniqKey="Lohela M" first="Marja" last="Lohela">Marja Lohela</name></noCountry><country name="Finlande"><region name="Uusimaa"><name sortKey="Alitalo, Kari" sort="Alitalo, Kari" uniqKey="Alitalo K" first="Kari" last="Alitalo">Kari Alitalo</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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