Alternatively spliced vascular endothelial growth factor receptor-2 is an essential endogenous inhibitor of lymphatic vessel growth.
Identifieur interne : 002D85 ( PubMed/Curation ); précédent : 002D84; suivant : 002D86Alternatively spliced vascular endothelial growth factor receptor-2 is an essential endogenous inhibitor of lymphatic vessel growth.
Auteurs : Romulo J C. Albuquerque [États-Unis] ; Takahiko Hayashi ; Won Gil Cho ; Mark E. Kleinman ; Sami Dridi ; Atsunobu Takeda ; Judit Z. Baffi ; Kiyoshi Yamada ; Hiroki Kaneko ; Martha G. Green ; Joe Chappell ; Jörg Wilting ; Herbert A. Weich ; Satoru Yamagami ; Shiro Amano ; Nobuhisa Mizuki ; Jonathan S. Alexander ; Martha L. Peterson ; Rolf A. Brekken ; Masanori Hirashima ; Seema Capoor ; Tomohiko Usui ; Balamurali K. Ambati ; Jayakrishna AmbatiSource :
- Nature medicine [ 1546-170X ] ; 2009.
Descripteurs français
- KwdFr :
- ADN complémentaire (génétique), Animaux, Animaux nouveau-nés, Cornée (), Cornée (croissance et développement), Cornée (métabolisme), Données de séquences moléculaires, Facteur de croissance endothéliale vasculaire de type C (antagonistes et inhibiteurs), Facteur de croissance endothéliale vasculaire de type C (physiologie), Humains, Lymphangiogenèse (génétique), Lymphangiogenèse (physiologie), Récepteur-2 au facteur croissance endothéliale vasculaire (déficit), Récepteur-2 au facteur croissance endothéliale vasculaire (génétique), Récepteur-2 au facteur croissance endothéliale vasculaire (physiologie), Souches mutantes de souris, Souris, Souris de lignée BALB C, Souris de lignée C57BL, Séquence nucléotidique, Vaisseaux lymphatiques (physiologie), Épissage alternatif.
- MESH :
- antagonistes et inhibiteurs : Facteur de croissance endothéliale vasculaire de type C.
- croissance et développement : Cornée.
- déficit : Récepteur-2 au facteur croissance endothéliale vasculaire.
- génétique : ADN complémentaire, Lymphangiogenèse, Récepteur-2 au facteur croissance endothéliale vasculaire.
- métabolisme : Cornée.
- physiologie : Facteur de croissance endothéliale vasculaire de type C, Lymphangiogenèse, Récepteur-2 au facteur croissance endothéliale vasculaire, Vaisseaux lymphatiques.
- Animaux, Animaux nouveau-nés, Cornée, Données de séquences moléculaires, Humains, Souches mutantes de souris, Souris, Souris de lignée BALB C, Souris de lignée C57BL, Séquence nucléotidique, Épissage alternatif.
English descriptors
- KwdEn :
- Alternative Splicing, Animals, Animals, Newborn, Base Sequence, Cornea (blood supply), Cornea (growth & development), Cornea (metabolism), DNA, Complementary (genetics), Humans, Lymphangiogenesis (genetics), Lymphangiogenesis (physiology), Lymphatic Vessels (physiology), Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Mutant Strains, Molecular Sequence Data, Vascular Endothelial Growth Factor C (antagonists & inhibitors), Vascular Endothelial Growth Factor C (physiology), Vascular Endothelial Growth Factor Receptor-2 (deficiency), Vascular Endothelial Growth Factor Receptor-2 (genetics), Vascular Endothelial Growth Factor Receptor-2 (physiology).
- MESH :
- chemical , antagonists & inhibitors : Vascular Endothelial Growth Factor C.
- chemical , deficiency : Vascular Endothelial Growth Factor Receptor-2.
- chemical , genetics : DNA, Complementary, Vascular Endothelial Growth Factor Receptor-2.
- blood supply : Cornea.
- genetics : Lymphangiogenesis.
- growth & development : Cornea.
- metabolism : Cornea.
- physiology : Lymphangiogenesis, Lymphatic Vessels, Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor Receptor-2.
- Alternative Splicing, Animals, Animals, Newborn, Base Sequence, Humans, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Mutant Strains, Molecular Sequence Data.
Abstract
Disruption of the precise balance of positive and negative molecular regulators of blood and lymphatic vessel growth can lead to myriad diseases. Although dozens of natural inhibitors of hemangiogenesis have been identified, an endogenous selective inhibitor of lymphatic vessel growth has not to our knowledge been previously described. We report the existence of a splice variant of the gene encoding vascular endothelial growth factor receptor-2 (Vegfr-2) that encodes a secreted form of the protein, designated soluble Vegfr-2 (sVegfr-2), that inhibits developmental and reparative lymphangiogenesis by blocking Vegf-c function. Tissue-specific loss of sVegfr-2 in mice induced, at birth, spontaneous lymphatic invasion of the normally alymphatic cornea and hyperplasia of skin lymphatics without affecting blood vasculature. Administration of sVegfr-2 inhibited lymphangiogenesis but not hemangiogenesis induced by corneal suture injury or transplantation, enhanced corneal allograft survival and suppressed lymphangioma cellular proliferation. Naturally occurring sVegfr-2 thus acts as a molecular uncoupler of blood and lymphatic vessels; modulation of sVegfr-2 might have therapeutic effects in treating lymphatic vascular malformations, transplantation rejection and, potentially, tumor lymphangiogenesis and lymphedema (pages 993-994).
DOI: 10.1038/nm.2018
PubMed: 19668192
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Albuquerque</name><affiliation wicri:level="1"><nlm:affiliation>Departments of Ophthalmology & Visual Sciences, Lexington, Kentucky, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Ophthalmology & Visual Sciences, Lexington, Kentucky</wicri:regionArea></affiliation></author><author><name sortKey="Hayashi, Takahiko" sort="Hayashi, Takahiko" uniqKey="Hayashi T" first="Takahiko" last="Hayashi">Takahiko Hayashi</name></author><author><name sortKey="Cho, Won Gil" sort="Cho, Won Gil" uniqKey="Cho W" first="Won Gil" last="Cho">Won Gil Cho</name></author><author><name sortKey="Kleinman, Mark E" sort="Kleinman, Mark E" uniqKey="Kleinman M" first="Mark E" last="Kleinman">Mark E. 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Albuquerque</name><affiliation wicri:level="1"><nlm:affiliation>Departments of Ophthalmology & Visual Sciences, Lexington, Kentucky, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Ophthalmology & Visual Sciences, Lexington, Kentucky</wicri:regionArea></affiliation></author><author><name sortKey="Hayashi, Takahiko" sort="Hayashi, Takahiko" uniqKey="Hayashi T" first="Takahiko" last="Hayashi">Takahiko Hayashi</name></author><author><name sortKey="Cho, Won Gil" sort="Cho, Won Gil" uniqKey="Cho W" first="Won Gil" last="Cho">Won Gil Cho</name></author><author><name sortKey="Kleinman, Mark E" sort="Kleinman, Mark E" uniqKey="Kleinman M" first="Mark E" last="Kleinman">Mark E. Kleinman</name></author><author><name sortKey="Dridi, Sami" sort="Dridi, Sami" uniqKey="Dridi S" first="Sami" last="Dridi">Sami Dridi</name></author><author><name sortKey="Takeda, Atsunobu" sort="Takeda, Atsunobu" uniqKey="Takeda A" first="Atsunobu" last="Takeda">Atsunobu Takeda</name></author><author><name sortKey="Baffi, Judit Z" sort="Baffi, Judit Z" uniqKey="Baffi J" first="Judit Z" last="Baffi">Judit Z. Baffi</name></author><author><name sortKey="Yamada, Kiyoshi" sort="Yamada, Kiyoshi" uniqKey="Yamada K" first="Kiyoshi" last="Yamada">Kiyoshi Yamada</name></author><author><name sortKey="Kaneko, Hiroki" sort="Kaneko, Hiroki" uniqKey="Kaneko H" first="Hiroki" last="Kaneko">Hiroki Kaneko</name></author><author><name sortKey="Green, Martha G" sort="Green, Martha G" uniqKey="Green M" first="Martha G" last="Green">Martha G. Green</name></author><author><name sortKey="Chappell, Joe" sort="Chappell, Joe" uniqKey="Chappell J" first="Joe" last="Chappell">Joe Chappell</name></author><author><name sortKey="Wilting, Jorg" sort="Wilting, Jorg" uniqKey="Wilting J" first="Jörg" last="Wilting">Jörg Wilting</name></author><author><name sortKey="Weich, Herbert A" sort="Weich, Herbert A" uniqKey="Weich H" first="Herbert A" last="Weich">Herbert A. Weich</name></author><author><name sortKey="Yamagami, Satoru" sort="Yamagami, Satoru" uniqKey="Yamagami S" first="Satoru" last="Yamagami">Satoru Yamagami</name></author><author><name sortKey="Amano, Shiro" sort="Amano, Shiro" uniqKey="Amano S" first="Shiro" last="Amano">Shiro Amano</name></author><author><name sortKey="Mizuki, Nobuhisa" sort="Mizuki, Nobuhisa" uniqKey="Mizuki N" first="Nobuhisa" last="Mizuki">Nobuhisa Mizuki</name></author><author><name sortKey="Alexander, Jonathan S" sort="Alexander, Jonathan S" uniqKey="Alexander J" first="Jonathan S" last="Alexander">Jonathan S. Alexander</name></author><author><name sortKey="Peterson, Martha L" sort="Peterson, Martha L" uniqKey="Peterson M" first="Martha L" last="Peterson">Martha L. Peterson</name></author><author><name sortKey="Brekken, Rolf A" sort="Brekken, Rolf A" uniqKey="Brekken R" first="Rolf A" last="Brekken">Rolf A. Brekken</name></author><author><name sortKey="Hirashima, Masanori" sort="Hirashima, Masanori" uniqKey="Hirashima M" first="Masanori" last="Hirashima">Masanori Hirashima</name></author><author><name sortKey="Capoor, Seema" sort="Capoor, Seema" uniqKey="Capoor S" first="Seema" last="Capoor">Seema Capoor</name></author><author><name sortKey="Usui, Tomohiko" sort="Usui, Tomohiko" uniqKey="Usui T" first="Tomohiko" last="Usui">Tomohiko Usui</name></author><author><name sortKey="Ambati, Balamurali K" sort="Ambati, Balamurali K" uniqKey="Ambati B" first="Balamurali K" last="Ambati">Balamurali K. Ambati</name></author><author><name sortKey="Ambati, Jayakrishna" sort="Ambati, Jayakrishna" uniqKey="Ambati J" first="Jayakrishna" last="Ambati">Jayakrishna Ambati</name></author></analytic><series><title level="j">Nature medicine</title><idno type="eISSN">1546-170X</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alternative Splicing</term><term>Animals</term><term>Animals, Newborn</term><term>Base Sequence</term><term>Cornea (blood supply)</term><term>Cornea (growth & development)</term><term>Cornea (metabolism)</term><term>DNA, Complementary (genetics)</term><term>Humans</term><term>Lymphangiogenesis (genetics)</term><term>Lymphangiogenesis (physiology)</term><term>Lymphatic Vessels (physiology)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred C57BL</term><term>Mice, Mutant Strains</term><term>Molecular Sequence Data</term><term>Vascular Endothelial Growth Factor C (antagonists & inhibitors)</term><term>Vascular Endothelial Growth Factor C (physiology)</term><term>Vascular Endothelial Growth Factor Receptor-2 (deficiency)</term><term>Vascular Endothelial Growth Factor Receptor-2 (genetics)</term><term>Vascular Endothelial Growth Factor Receptor-2 (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ADN complémentaire (génétique)</term><term>Animaux</term><term>Animaux nouveau-nés</term><term>Cornée ()</term><term>Cornée (croissance et développement)</term><term>Cornée (métabolisme)</term><term>Données de séquences moléculaires</term><term>Facteur de croissance endothéliale vasculaire de type C (antagonistes et inhibiteurs)</term><term>Facteur de croissance endothéliale vasculaire de type C (physiologie)</term><term>Humains</term><term>Lymphangiogenèse (génétique)</term><term>Lymphangiogenèse (physiologie)</term><term>Récepteur-2 au facteur croissance endothéliale vasculaire (déficit)</term><term>Récepteur-2 au facteur croissance endothéliale vasculaire (génétique)</term><term>Récepteur-2 au facteur croissance endothéliale vasculaire (physiologie)</term><term>Souches mutantes de souris</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Souris de lignée C57BL</term><term>Séquence nucléotidique</term><term>Vaisseaux lymphatiques (physiologie)</term><term>Épissage alternatif</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Vascular Endothelial Growth Factor C</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Vascular Endothelial Growth Factor Receptor-2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA, Complementary</term><term>Vascular Endothelial Growth Factor Receptor-2</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type C</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Cornea</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Cornée</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Récepteur-2 au facteur croissance endothéliale vasculaire</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lymphangiogenesis</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Cornea</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ADN complémentaire</term><term>Lymphangiogenèse</term><term>Récepteur-2 au facteur croissance endothéliale vasculaire</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cornea</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cornée</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type C</term><term>Lymphangiogenèse</term><term>Récepteur-2 au facteur croissance endothéliale vasculaire</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymphangiogenesis</term><term>Lymphatic Vessels</term><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factor Receptor-2</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Alternative Splicing</term><term>Animals</term><term>Animals, Newborn</term><term>Base Sequence</term><term>Humans</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred C57BL</term><term>Mice, Mutant Strains</term><term>Molecular Sequence Data</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Animaux nouveau-nés</term><term>Cornée</term><term>Données de séquences moléculaires</term><term>Humains</term><term>Souches mutantes de souris</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Souris de lignée C57BL</term><term>Séquence nucléotidique</term><term>Épissage alternatif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Disruption of the precise balance of positive and negative molecular regulators of blood and lymphatic vessel growth can lead to myriad diseases. Although dozens of natural inhibitors of hemangiogenesis have been identified, an endogenous selective inhibitor of lymphatic vessel growth has not to our knowledge been previously described. We report the existence of a splice variant of the gene encoding vascular endothelial growth factor receptor-2 (Vegfr-2) that encodes a secreted form of the protein, designated soluble Vegfr-2 (sVegfr-2), that inhibits developmental and reparative lymphangiogenesis by blocking Vegf-c function. Tissue-specific loss of sVegfr-2 in mice induced, at birth, spontaneous lymphatic invasion of the normally alymphatic cornea and hyperplasia of skin lymphatics without affecting blood vasculature. Administration of sVegfr-2 inhibited lymphangiogenesis but not hemangiogenesis induced by corneal suture injury or transplantation, enhanced corneal allograft survival and suppressed lymphangioma cellular proliferation. Naturally occurring sVegfr-2 thus acts as a molecular uncoupler of blood and lymphatic vessels; modulation of sVegfr-2 might have therapeutic effects in treating lymphatic vascular malformations, transplantation rejection and, potentially, tumor lymphangiogenesis and lymphedema (pages 993-994).</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19668192</PMID><DateCreated><Year>2009</Year><Month>09</Month><Day>07</Day></DateCreated><DateCompleted><Year>2009</Year><Month>10</Month><Day>02</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1546-170X</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><Issue>9</Issue><PubDate><Year>2009</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Nature medicine</Title><ISOAbbreviation>Nat. Med.</ISOAbbreviation></Journal><ArticleTitle>Alternatively spliced vascular endothelial growth factor receptor-2 is an essential endogenous inhibitor of lymphatic vessel growth.</ArticleTitle><Pagination><MedlinePgn>1023-30</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/nm.2018</ELocationID><Abstract><AbstractText>Disruption of the precise balance of positive and negative molecular regulators of blood and lymphatic vessel growth can lead to myriad diseases. Although dozens of natural inhibitors of hemangiogenesis have been identified, an endogenous selective inhibitor of lymphatic vessel growth has not to our knowledge been previously described. We report the existence of a splice variant of the gene encoding vascular endothelial growth factor receptor-2 (Vegfr-2) that encodes a secreted form of the protein, designated soluble Vegfr-2 (sVegfr-2), that inhibits developmental and reparative lymphangiogenesis by blocking Vegf-c function. Tissue-specific loss of sVegfr-2 in mice induced, at birth, spontaneous lymphatic invasion of the normally alymphatic cornea and hyperplasia of skin lymphatics without affecting blood vasculature. Administration of sVegfr-2 inhibited lymphangiogenesis but not hemangiogenesis induced by corneal suture injury or transplantation, enhanced corneal allograft survival and suppressed lymphangioma cellular proliferation. Naturally occurring sVegfr-2 thus acts as a molecular uncoupler of blood and lymphatic vessels; modulation of sVegfr-2 might have therapeutic effects in treating lymphatic vascular malformations, transplantation rejection and, potentially, tumor lymphangiogenesis and lymphedema (pages 993-994).</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Albuquerque</LastName><ForeName>Romulo J C</ForeName><Initials>RJ</Initials><AffiliationInfo><Affiliation>Departments of Ophthalmology & Visual Sciences, Lexington, Kentucky, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hayashi</LastName><ForeName>Takahiko</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Cho</LastName><ForeName>Won Gil</ForeName><Initials>WG</Initials></Author><Author ValidYN="Y"><LastName>Kleinman</LastName><ForeName>Mark E</ForeName><Initials>ME</Initials></Author><Author ValidYN="Y"><LastName>Dridi</LastName><ForeName>Sami</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Takeda</LastName><ForeName>Atsunobu</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Baffi</LastName><ForeName>Judit Z</ForeName><Initials>JZ</Initials></Author><Author ValidYN="Y"><LastName>Yamada</LastName><ForeName>Kiyoshi</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Kaneko</LastName><ForeName>Hiroki</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Green</LastName><ForeName>Martha G</ForeName><Initials>MG</Initials></Author><Author ValidYN="Y"><LastName>Chappell</LastName><ForeName>Joe</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Wilting</LastName><ForeName>Jörg</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Weich</LastName><ForeName>Herbert A</ForeName><Initials>HA</Initials></Author><Author ValidYN="Y"><LastName>Yamagami</LastName><ForeName>Satoru</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Amano</LastName><ForeName>Shiro</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Mizuki</LastName><ForeName>Nobuhisa</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Alexander</LastName><ForeName>Jonathan S</ForeName><Initials>JS</Initials></Author><Author ValidYN="Y"><LastName>Peterson</LastName><ForeName>Martha L</ForeName><Initials>ML</Initials></Author><Author ValidYN="Y"><LastName>Brekken</LastName><ForeName>Rolf A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Hirashima</LastName><ForeName>Masanori</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Capoor</LastName><ForeName>Seema</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Usui</LastName><ForeName>Tomohiko</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Ambati</LastName><ForeName>Balamurali K</ForeName><Initials>BK</Initials></Author><Author ValidYN="Y"><LastName>Ambati</LastName><ForeName>Jayakrishna</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>GENBANK</DataBankName><AccessionNumberList><AccessionNumber>EU884114</AccessionNumber><AccessionNumber>FJ899739</AccessionNumber></AccessionNumberList></DataBank></DataBankList><GrantList CompleteYN="Y"><Grant><GrantID>EY017182</GrantID><Acronym>EY</Acronym><Agency>NEI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>EY015422</GrantID><Acronym>EY</Acronym><Agency>NEI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 EY017182</GrantID><Acronym>EY</Acronym><Agency>NEI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>RC1 EY020442</GrantID><Acronym>EY</Acronym><Agency>NEI NIH HHS</Agency><Country>United 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