Deletion of Vascular Endothelial Growth Factor C (VEGF-C) and VEGF-D Is Not Equivalent to VEGF Receptor 3 Deletion in Mouse Embryos▿
Identifieur interne : 006B60 ( Main/Exploration ); précédent : 006B59; suivant : 006B61Deletion of Vascular Endothelial Growth Factor C (VEGF-C) and VEGF-D Is Not Equivalent to VEGF Receptor 3 Deletion in Mouse Embryos▿
Auteurs : Paula Haiko ; Taija Makinen ; Salla Keskitalo ; Jussi Taipale ; Marika J. Karkkainen ; Megan E. Baldwin ; Steven A. Stacker ; Marc G. Achen ; Kari Alitalo [Finlande]Source :
- Molecular and Cellular Biology [ 0270-7306 ] ; 2008.
Descripteurs français
- KwdFr :
- Allèles, Animaux, Ciblage de gène, Délétion de gène, Embryon de mammifère (anatomopathologie), Embryon de mammifère (malformations), Embryon de mammifère (métabolisme), Facteur de croissance endothéliale vasculaire de type C (déficit), Facteur de croissance endothéliale vasculaire de type D (déficit), Lymphangiogenèse, Phénotype, Récepteur-3 au facteur croissance endothéliale vasculaire (déficit), Souris, Souris knockout, Vaisseaux lymphatiques (anatomopathologie), Vaisseaux lymphatiques (embryologie), Vaisseaux lymphatiques (malformations), Vaisseaux sanguins (embryologie).
- MESH :
- anatomopathologie : Embryon de mammifère, Vaisseaux lymphatiques.
- déficit : Facteur de croissance endothéliale vasculaire de type C, Facteur de croissance endothéliale vasculaire de type D, Récepteur-3 au facteur croissance endothéliale vasculaire.
- embryologie : Vaisseaux lymphatiques, Vaisseaux sanguins.
- malformations : Embryon de mammifère, Vaisseaux lymphatiques.
- métabolisme : Embryon de mammifère.
- Allèles, Animaux, Ciblage de gène, Délétion de gène, Lymphangiogenèse, Phénotype, Souris, Souris knockout.
English descriptors
- KwdEn :
- Alleles, Animals, Blood Vessels (embryology), Embryo, Mammalian (abnormalities), Embryo, Mammalian (metabolism), Embryo, Mammalian (pathology), Gene Deletion, Gene Targeting, Lymphangiogenesis, Lymphatic Vessels (abnormalities), Lymphatic Vessels (embryology), Lymphatic Vessels (pathology), Mice, Mice, Knockout, Phenotype, Vascular Endothelial Growth Factor C (deficiency), Vascular Endothelial Growth Factor D (deficiency), Vascular Endothelial Growth Factor Receptor-3 (deficiency).
- MESH :
- chemical , deficiency : Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor D, Vascular Endothelial Growth Factor Receptor-3.
- abnormalities : Embryo, Mammalian, Lymphatic Vessels.
- embryology : Blood Vessels, Lymphatic Vessels.
- metabolism : Embryo, Mammalian.
- pathology : Embryo, Mammalian, Lymphatic Vessels.
- Alleles, Animals, Gene Deletion, Gene Targeting, Lymphangiogenesis, Mice, Mice, Knockout, Phenotype.
Abstract
Lymphatic vessels play an important role in the regulation of tissue fluid balance, immune responses, and fat adsorption and are involved in diseases including lymphedema and tumor metastasis. Vascular endothelial growth factor (VEGF) receptor 3 (VEGFR-3) is necessary for development of the blood vasculature during early embryogenesis, but later, VEGFR-3 expression becomes restricted to the lymphatic vasculature. We analyzed mice deficient in both of the known VEGFR-3 ligands, VEGF-C and VEGF-D. Unlike the
Url:
DOI: 10.1128/MCB.02214-07
PubMed: 18519586
PubMed Central: 2493372
Affiliations:
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Karkkainen</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Baldwin, Megan E" sort="Baldwin, Megan E" uniqKey="Baldwin M" first="Megan E." last="Baldwin">Megan E. Baldwin</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Stacker, Steven A" sort="Stacker, Steven A" uniqKey="Stacker S" first="Steven A." last="Stacker">Steven A. Stacker</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Achen, Marc G" sort="Achen, Marc G" uniqKey="Achen M" first="Marc G." last="Achen">Marc G. Achen</name><affiliation><nlm:aff id="aff1"></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="aff1"></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">Molecular and Cellular Biology</title><idno type="ISSN">0270-7306</idno><idno type="eISSN">1098-5549</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alleles</term><term>Animals</term><term>Blood Vessels (embryology)</term><term>Embryo, Mammalian (abnormalities)</term><term>Embryo, Mammalian (metabolism)</term><term>Embryo, Mammalian (pathology)</term><term>Gene Deletion</term><term>Gene Targeting</term><term>Lymphangiogenesis</term><term>Lymphatic Vessels (abnormalities)</term><term>Lymphatic Vessels (embryology)</term><term>Lymphatic Vessels (pathology)</term><term>Mice</term><term>Mice, Knockout</term><term>Phenotype</term><term>Vascular Endothelial Growth Factor C (deficiency)</term><term>Vascular Endothelial Growth Factor D (deficiency)</term><term>Vascular Endothelial Growth Factor Receptor-3 (deficiency)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Allèles</term><term>Animaux</term><term>Ciblage de gène</term><term>Délétion de gène</term><term>Embryon de mammifère (anatomopathologie)</term><term>Embryon de mammifère (malformations)</term><term>Embryon de mammifère (métabolisme)</term><term>Facteur de croissance endothéliale vasculaire de type C (déficit)</term><term>Facteur de croissance endothéliale vasculaire de type D (déficit)</term><term>Lymphangiogenèse</term><term>Phénotype</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (déficit)</term><term>Souris</term><term>Souris knockout</term><term>Vaisseaux lymphatiques (anatomopathologie)</term><term>Vaisseaux lymphatiques (embryologie)</term><term>Vaisseaux lymphatiques (malformations)</term><term>Vaisseaux sanguins (embryologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><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" qualifier="abnormalities" xml:lang="en"><term>Embryo, Mammalian</term><term>Lymphatic Vessels</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Embryon de mammifère</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type C</term><term>Facteur de croissance endothéliale vasculaire de type D</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term></keywords><keywords scheme="MESH" qualifier="embryologie" xml:lang="fr"><term>Vaisseaux lymphatiques</term><term>Vaisseaux sanguins</term></keywords><keywords scheme="MESH" qualifier="embryology" xml:lang="en"><term>Blood Vessels</term><term>Lymphatic Vessels</term></keywords><keywords scheme="MESH" qualifier="malformations" xml:lang="fr"><term>Embryon de mammifère</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Embryo, Mammalian</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Embryon de mammifère</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Embryo, Mammalian</term><term>Lymphatic Vessels</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Alleles</term><term>Animals</term><term>Gene Deletion</term><term>Gene Targeting</term><term>Lymphangiogenesis</term><term>Mice</term><term>Mice, Knockout</term><term>Phenotype</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Allèles</term><term>Animaux</term><term>Ciblage de gène</term><term>Délétion de gène</term><term>Lymphangiogenèse</term><term>Phénotype</term><term>Souris</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Lymphatic vessels play an important role in the regulation of tissue fluid balance, immune responses, and fat adsorption and are involved in diseases including lymphedema and tumor metastasis. Vascular endothelial growth factor (VEGF) receptor 3 (VEGFR-3) is necessary for development of the blood vasculature during early embryogenesis, but later, VEGFR-3 expression becomes restricted to the lymphatic vasculature. We analyzed mice deficient in both of the known VEGFR-3 ligands, VEGF-C and VEGF-D. Unlike the <italic>Vegfr3</italic><sup>−/−</sup> embryos, the <italic>Vegfc</italic><sup>−/−</sup>; <italic>Vegfd</italic><sup>−/−</sup> embryos displayed normal blood vasculature after embryonic day 9.5. Deletion of <italic>Vegfr3</italic> in the epiblast, using keratin 19 (K19) Cre, resulted in a phenotype identical to that of the <italic>Vegfr3</italic><sup>−/−</sup> embryos, suggesting that this phenotype is due to defects in the embryo proper and not in placental development. Interestingly, the <italic>Vegfr3</italic><sup><italic>neo</italic></sup> hypomorphic mutant mice carrying the neomycin cassette between exons 1 and 2 showed defective lymphatic development. Overexpression of human or mouse VEGF-D in the skin, under the K14 promoter, rescued the lymphatic hypoplasia of the <italic>Vegfc</italic><sup>+/−</sup> mice in the K14-VEGF-D; <italic>Vegfc</italic><sup>+/−</sup> compound mice, suggesting that VEGF-D is functionally redundant with VEGF-C in the stimulation of developmental lymphangiogenesis. Our results suggest VEGF-C- and VEGF-D-independent functions for VEGFR-3 in the early embryo.</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="Achen, Marc G" sort="Achen, Marc G" uniqKey="Achen M" first="Marc G." last="Achen">Marc G. Achen</name><name sortKey="Baldwin, Megan E" sort="Baldwin, Megan E" uniqKey="Baldwin M" first="Megan E." last="Baldwin">Megan E. Baldwin</name><name sortKey="Haiko, Paula" sort="Haiko, Paula" uniqKey="Haiko P" first="Paula" last="Haiko">Paula Haiko</name><name sortKey="Karkkainen, Marika J" sort="Karkkainen, Marika J" uniqKey="Karkkainen M" first="Marika J." last="Karkkainen">Marika J. Karkkainen</name><name sortKey="Keskitalo, Salla" sort="Keskitalo, Salla" uniqKey="Keskitalo S" first="Salla" last="Keskitalo">Salla Keskitalo</name><name sortKey="Makinen, Taija" sort="Makinen, Taija" uniqKey="Makinen T" first="Taija" last="Makinen">Taija Makinen</name><name sortKey="Stacker, Steven A" sort="Stacker, Steven A" uniqKey="Stacker S" first="Steven A." last="Stacker">Steven A. Stacker</name><name sortKey="Taipale, Jussi" sort="Taipale, Jussi" uniqKey="Taipale J" first="Jussi" last="Taipale">Jussi Taipale</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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