Role of VEGF-D and VEGFR-3 in developmental lymphangiogenesis, a chemicogenetic study in Xenopus tadpoles.
Identifieur interne : 002E64 ( PubMed/Checkpoint ); précédent : 002E63; suivant : 002E65Role of VEGF-D and VEGFR-3 in developmental lymphangiogenesis, a chemicogenetic study in Xenopus tadpoles.
Auteurs : Annelii Ny [Belgique] ; Marta Koch ; Wouter Vandevelde ; Martin Schneider ; Christian Fischer ; Antonio Diez-Juan ; Elke Neven ; Ilse Geudens ; Sunit Maity ; Lieve Moons ; Stéphane Plaisance ; Diether Lambrechts ; Peter Carmeliet ; Mieke DewerchinSource :
- Blood [ 1528-0020 ] ; 2008.
Descripteurs français
- KwdFr :
- Animaux, Extinction de l'expression des gènes, Facteur de croissance endothéliale vasculaire de type D (antagonistes et inhibiteurs), Facteur de croissance endothéliale vasculaire de type D (génétique), Facteur de croissance endothéliale vasculaire de type D (physiologie), Larve (croissance et développement), Lymphangiogenèse (génétique), Lymphangiogenèse (physiologie), Oligodésoxyribonucléotides antisens (génétique), Protéines de Xénope (génétique), Protéines de Xénope (physiologie), Récepteur-3 au facteur croissance endothéliale vasculaire (antagonistes et inhibiteurs), Récepteur-3 au facteur croissance endothéliale vasculaire (génétique), Récepteur-3 au facteur croissance endothéliale vasculaire (physiologie), Vaisseaux lymphatiques (embryologie), Vaisseaux lymphatiques (malformations), Xenopus laevis (croissance et développement), Xenopus laevis (embryologie), Xenopus laevis (génétique), Xenopus laevis (physiologie).
- MESH :
- antagonistes et inhibiteurs : Facteur de croissance endothéliale vasculaire de type D, Récepteur-3 au facteur croissance endothéliale vasculaire.
- croissance et développement : Larve, Xenopus laevis.
- embryologie : Vaisseaux lymphatiques, Xenopus laevis.
- génétique : Facteur de croissance endothéliale vasculaire de type D, Lymphangiogenèse, Oligodésoxyribonucléotides antisens, Protéines de Xénope, Récepteur-3 au facteur croissance endothéliale vasculaire, Xenopus laevis.
- malformations : Vaisseaux lymphatiques.
- physiologie : Facteur de croissance endothéliale vasculaire de type D, Lymphangiogenèse, Protéines de Xénope, Récepteur-3 au facteur croissance endothéliale vasculaire, Xenopus laevis.
- Animaux, Extinction de l'expression des gènes.
English descriptors
- KwdEn :
- Animals, Gene Silencing, Larva (growth & development), Lymphangiogenesis (genetics), Lymphangiogenesis (physiology), Lymphatic Vessels (abnormalities), Lymphatic Vessels (embryology), Oligodeoxyribonucleotides, Antisense (genetics), Vascular Endothelial Growth Factor D (antagonists & inhibitors), Vascular Endothelial Growth Factor D (genetics), Vascular Endothelial Growth Factor D (physiology), Vascular Endothelial Growth Factor Receptor-3 (antagonists & inhibitors), Vascular Endothelial Growth Factor Receptor-3 (genetics), Vascular Endothelial Growth Factor Receptor-3 (physiology), Xenopus Proteins (genetics), Xenopus Proteins (physiology), Xenopus laevis (embryology), Xenopus laevis (genetics), Xenopus laevis (growth & development), Xenopus laevis (physiology).
- MESH :
- chemical , antagonists & inhibitors : Vascular Endothelial Growth Factor D, Vascular Endothelial Growth Factor Receptor-3.
- chemical , genetics : Oligodeoxyribonucleotides, Antisense, Vascular Endothelial Growth Factor D, Vascular Endothelial Growth Factor Receptor-3, Xenopus Proteins.
- abnormalities : Lymphatic Vessels.
- embryology : Lymphatic Vessels, Xenopus laevis.
- genetics : Lymphangiogenesis, Xenopus laevis.
- growth & development : Larva, Xenopus laevis.
- physiology : Lymphangiogenesis, Vascular Endothelial Growth Factor D, Vascular Endothelial Growth Factor Receptor-3, Xenopus Proteins, Xenopus laevis.
- Animals, Gene Silencing.
Abstract
The importance of the lymphangiogenic factor VEGF-D and its receptor VEGFR-3 in early lymphatic development remains largely unresolved. We therefore investigated their role in Xenopus laevis tadpoles, a small animal model allowing chemicogenetic dissection of developmental lymphangiogenesis. Single morpholino antisense oligo knockdown of xVEGF-D did not affect lymphatic commitment, but transiently impaired lymphatic endothelial cell (LEC) migration. Notably, combined knockdown of xVEGF-D with xVEGF-C at suboptimal morpholino concentrations resulted in more severe migration defects and lymphedema formation than the corresponding single knockdowns. Knockdown of VEGFR-3 or treatment with the VEGFR-3 inhibitor MAZ51 similarly impaired lymph vessel formation and function and caused pronounced edema. VEGFR-3 silencing by morpholino knockdown, MAZ51 treatment, or xVEGF-C/D double knockdown also resulted in dilation and dysfunction of the lymph heart. These findings document a critical role of VEGFR-3 in embryonic lymphatic development and function, and reveal a previously unrecognized modifier role of VEGF-D in the regulation of embryonic lymphangiogenesis in frog embryos.
DOI: 10.1182/blood-2007-08-106302
PubMed: 18474726
Affiliations:
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pubmed:18474726Le document en format XML
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& development)</term><term>Lymphangiogenesis (genetics)</term><term>Lymphangiogenesis (physiology)</term><term>Lymphatic Vessels (abnormalities)</term><term>Lymphatic Vessels (embryology)</term><term>Oligodeoxyribonucleotides, Antisense (genetics)</term><term>Vascular Endothelial Growth Factor D (antagonists & inhibitors)</term><term>Vascular Endothelial Growth Factor D (genetics)</term><term>Vascular Endothelial Growth Factor D (physiology)</term><term>Vascular Endothelial Growth Factor Receptor-3 (antagonists & inhibitors)</term><term>Vascular Endothelial Growth Factor Receptor-3 (genetics)</term><term>Vascular Endothelial Growth Factor Receptor-3 (physiology)</term><term>Xenopus Proteins (genetics)</term><term>Xenopus Proteins (physiology)</term><term>Xenopus laevis (embryology)</term><term>Xenopus laevis (genetics)</term><term>Xenopus laevis (growth & development)</term><term>Xenopus laevis (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Extinction de l'expression des gènes</term><term>Facteur de croissance endothéliale vasculaire de type D (antagonistes et inhibiteurs)</term><term>Facteur de croissance endothéliale vasculaire de type D (génétique)</term><term>Facteur de croissance endothéliale vasculaire de type D (physiologie)</term><term>Larve (croissance et développement)</term><term>Lymphangiogenèse (génétique)</term><term>Lymphangiogenèse (physiologie)</term><term>Oligodésoxyribonucléotides antisens (génétique)</term><term>Protéines de Xénope (génétique)</term><term>Protéines de Xénope (physiologie)</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (antagonistes et inhibiteurs)</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (génétique)</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (physiologie)</term><term>Vaisseaux lymphatiques (embryologie)</term><term>Vaisseaux lymphatiques (malformations)</term><term>Xenopus laevis (croissance et développement)</term><term>Xenopus laevis (embryologie)</term><term>Xenopus laevis (génétique)</term><term>Xenopus laevis (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Vascular Endothelial Growth Factor D</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Oligodeoxyribonucleotides, Antisense</term><term>Vascular Endothelial Growth Factor D</term><term>Vascular Endothelial Growth Factor Receptor-3</term><term>Xenopus Proteins</term></keywords><keywords scheme="MESH" qualifier="abnormalities" xml:lang="en"><term>Lymphatic Vessels</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type D</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Larve</term><term>Xenopus laevis</term></keywords><keywords scheme="MESH" qualifier="embryologie" xml:lang="fr"><term>Vaisseaux lymphatiques</term><term>Xenopus laevis</term></keywords><keywords scheme="MESH" qualifier="embryology" xml:lang="en"><term>Lymphatic Vessels</term><term>Xenopus laevis</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lymphangiogenesis</term><term>Xenopus laevis</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Larva</term><term>Xenopus laevis</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type D</term><term>Lymphangiogenèse</term><term>Oligodésoxyribonucléotides antisens</term><term>Protéines de Xénope</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term><term>Xenopus laevis</term></keywords><keywords scheme="MESH" qualifier="malformations" xml:lang="fr"><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type D</term><term>Lymphangiogenèse</term><term>Protéines de Xénope</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term><term>Xenopus laevis</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymphangiogenesis</term><term>Vascular Endothelial Growth Factor D</term><term>Vascular Endothelial Growth Factor Receptor-3</term><term>Xenopus Proteins</term><term>Xenopus laevis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Silencing</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Extinction de l'expression des gènes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The importance of the lymphangiogenic factor VEGF-D and its receptor VEGFR-3 in early lymphatic development remains largely unresolved. We therefore investigated their role in Xenopus laevis tadpoles, a small animal model allowing chemicogenetic dissection of developmental lymphangiogenesis. Single morpholino antisense oligo knockdown of xVEGF-D did not affect lymphatic commitment, but transiently impaired lymphatic endothelial cell (LEC) migration. Notably, combined knockdown of xVEGF-D with xVEGF-C at suboptimal morpholino concentrations resulted in more severe migration defects and lymphedema formation than the corresponding single knockdowns. Knockdown of VEGFR-3 or treatment with the VEGFR-3 inhibitor MAZ51 similarly impaired lymph vessel formation and function and caused pronounced edema. VEGFR-3 silencing by morpholino knockdown, MAZ51 treatment, or xVEGF-C/D double knockdown also resulted in dilation and dysfunction of the lymph heart. These findings document a critical role of VEGFR-3 in embryonic lymphatic development and function, and reveal a previously unrecognized modifier role of VEGF-D in the regulation of embryonic lymphangiogenesis in frog embryos.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18474726</PMID><DateCreated><Year>2008</Year><Month>08</Month><Day>26</Day></DateCreated><DateCompleted><Year>2008</Year><Month>09</Month><Day>30</Day></DateCompleted><DateRevised><Year>2009</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1528-0020</ISSN><JournalIssue CitedMedium="Internet"><Volume>112</Volume><Issue>5</Issue><PubDate><Year>2008</Year><Month>Sep</Month><Day>01</Day></PubDate></JournalIssue><Title>Blood</Title><ISOAbbreviation>Blood</ISOAbbreviation></Journal><ArticleTitle>Role of VEGF-D and VEGFR-3 in developmental lymphangiogenesis, a chemicogenetic study in Xenopus tadpoles.</ArticleTitle><Pagination><MedlinePgn>1740-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1182/blood-2007-08-106302</ELocationID><Abstract><AbstractText>The importance of the lymphangiogenic factor VEGF-D and its receptor VEGFR-3 in early lymphatic development remains largely unresolved. We therefore investigated their role in Xenopus laevis tadpoles, a small animal model allowing chemicogenetic dissection of developmental lymphangiogenesis. Single morpholino antisense oligo knockdown of xVEGF-D did not affect lymphatic commitment, but transiently impaired lymphatic endothelial cell (LEC) migration. Notably, combined knockdown of xVEGF-D with xVEGF-C at suboptimal morpholino concentrations resulted in more severe migration defects and lymphedema formation than the corresponding single knockdowns. Knockdown of VEGFR-3 or treatment with the VEGFR-3 inhibitor MAZ51 similarly impaired lymph vessel formation and function and caused pronounced edema. VEGFR-3 silencing by morpholino knockdown, MAZ51 treatment, or xVEGF-C/D double knockdown also resulted in dilation and dysfunction of the lymph heart. These findings document a critical role of VEGFR-3 in embryonic lymphatic development and function, and reveal a previously unrecognized modifier role of VEGF-D in the regulation of embryonic lymphangiogenesis in frog embryos.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ny</LastName><ForeName>Annelii</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Vesalius Research Center, VIB-KU Leuven, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Koch</LastName><ForeName>Marta</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Vandevelde</LastName><ForeName>Wouter</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Schneider</LastName><ForeName>Martin</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Fischer</LastName><ForeName>Christian</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Diez-Juan</LastName><ForeName>Antonio</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Neven</LastName><ForeName>Elke</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Geudens</LastName><ForeName>Ilse</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Maity</LastName><ForeName>Sunit</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Moons</LastName><ForeName>Lieve</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Plaisance</LastName><ForeName>Stéphane</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Lambrechts</LastName><ForeName>Diether</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Carmeliet</LastName><ForeName>Peter</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Dewerchin</LastName><ForeName>Mieke</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2008</Year><Month>05</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Blood</MedlineTA><NlmUniqueID>7603509</NlmUniqueID><ISSNLinking>0006-4971</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020319">Oligodeoxyribonucleotides, Antisense</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042643">Vascular Endothelial Growth Factor D</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029867">Xenopus Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D040321">Vascular Endothelial Growth Factor Receptor-3</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Blood. 2008 Sep 1;112(5):1547-8</RefSource><PMID Version="1">18725566</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020868" MajorTopicYN="N">Gene Silencing</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007814" MajorTopicYN="N">Larva</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName><QualifierName UI="Q000002" MajorTopicYN="N">abnormalities</QualifierName><QualifierName UI="Q000196" MajorTopicYN="N">embryology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020319" MajorTopicYN="N">Oligodeoxyribonucleotides, Antisense</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042643" MajorTopicYN="N">Vascular Endothelial Growth Factor D</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D040321" MajorTopicYN="N">Vascular Endothelial Growth Factor Receptor-3</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029867" MajorTopicYN="N">Xenopus Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014982" MajorTopicYN="N">Xenopus laevis</DescriptorName><QualifierName UI="Q000196" MajorTopicYN="N">embryology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>5</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>10</Month><Day>1</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>5</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">18474726</ArticleId><ArticleId IdType="pii">blood-2007-08-106302</ArticleId><ArticleId IdType="doi">10.1182/blood-2007-08-106302</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Belgique</li></country></list><tree><noCountry><name sortKey="Carmeliet, Peter" sort="Carmeliet, Peter" uniqKey="Carmeliet P" first="Peter" last="Carmeliet">Peter Carmeliet</name><name sortKey="Dewerchin, Mieke" sort="Dewerchin, Mieke" uniqKey="Dewerchin M" first="Mieke" last="Dewerchin">Mieke Dewerchin</name><name sortKey="Diez Juan, Antonio" sort="Diez Juan, Antonio" uniqKey="Diez Juan A" first="Antonio" last="Diez-Juan">Antonio Diez-Juan</name><name sortKey="Fischer, Christian" sort="Fischer, Christian" uniqKey="Fischer C" first="Christian" last="Fischer">Christian Fischer</name><name sortKey="Geudens, Ilse" sort="Geudens, Ilse" uniqKey="Geudens I" first="Ilse" last="Geudens">Ilse Geudens</name><name sortKey="Koch, Marta" sort="Koch, Marta" uniqKey="Koch M" first="Marta" last="Koch">Marta Koch</name><name sortKey="Lambrechts, Diether" sort="Lambrechts, Diether" uniqKey="Lambrechts D" first="Diether" last="Lambrechts">Diether Lambrechts</name><name sortKey="Maity, Sunit" sort="Maity, Sunit" uniqKey="Maity S" first="Sunit" last="Maity">Sunit Maity</name><name sortKey="Moons, Lieve" sort="Moons, Lieve" uniqKey="Moons L" first="Lieve" last="Moons">Lieve Moons</name><name sortKey="Neven, Elke" sort="Neven, Elke" uniqKey="Neven E" first="Elke" last="Neven">Elke Neven</name><name sortKey="Plaisance, Stephane" sort="Plaisance, Stephane" uniqKey="Plaisance S" first="Stéphane" last="Plaisance">Stéphane Plaisance</name><name sortKey="Schneider, Martin" sort="Schneider, Martin" uniqKey="Schneider M" first="Martin" last="Schneider">Martin Schneider</name><name sortKey="Vandevelde, Wouter" sort="Vandevelde, Wouter" uniqKey="Vandevelde W" first="Wouter" last="Vandevelde">Wouter Vandevelde</name></noCountry><country name="Belgique"><noRegion><name sortKey="Ny, Annelii" sort="Ny, Annelii" uniqKey="Ny A" first="Annelii" last="Ny">Annelii Ny</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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