CCBE1 enhances lymphangiogenesis via A disintegrin and metalloprotease with thrombospondin motifs-3-mediated vascular endothelial growth factor-C activation.
Identifieur interne : 001669 ( PubMed/Curation ); précédent : 001668; suivant : 001670CCBE1 enhances lymphangiogenesis via A disintegrin and metalloprotease with thrombospondin motifs-3-mediated vascular endothelial growth factor-C activation.
Auteurs : Michael Jeltsch [Finlande] ; Sawan Kumar Jha ; Denis Tvorogov ; Andrey Anisimov ; Veli-Matti Lepp Nen ; Tanja Holopainen ; Riikka Kivel ; Sagrario Ortega ; Terhi K Rpanen ; Kari AlitaloSource :
- Circulation [ 1524-4539 ] ; 2014.
Descripteurs français
- KwdFr :
- Adenoviridae (génétique), Animaux, Cellules HEK293, Cellules cultivées, Endothélium vasculaire (cytologie), Endothélium vasculaire (métabolisme), Facteur de croissance endothéliale vasculaire de type C (métabolisme), Humains, Lignées consanguines de souris, Lymphangiogenèse (physiologie), Modèles animaux, Muscles squelettiques (), Muscles squelettiques (métabolisme), Mâle, Néovascularisation physiologique (physiologie), Procollagen peptidase (métabolisme), Protéines ADAM (métabolisme), Protéines ADAMTS, Protéines de liaison au calcium (génétique), Protéines de liaison au calcium (métabolisme), Protéines suppresseurs de tumeurs (génétique), Protéines suppresseurs de tumeurs (métabolisme), Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme), Souris, Techniques in vitro, Transfection.
- MESH :
- cytologie : Endothélium vasculaire.
- génétique : Adenoviridae, Protéines de liaison au calcium, Protéines suppresseurs de tumeurs.
- métabolisme : Endothélium vasculaire, Facteur de croissance endothéliale vasculaire de type C, Muscles squelettiques, Procollagen peptidase, Protéines ADAM, Protéines de liaison au calcium, Protéines suppresseurs de tumeurs, Récepteur-3 au facteur croissance endothéliale vasculaire.
- physiologie : Lymphangiogenèse, Néovascularisation physiologique.
- Animaux, Cellules HEK293, Cellules cultivées, Humains, Lignées consanguines de souris, Modèles animaux, Muscles squelettiques, Mâle, Protéines ADAMTS, Souris, Techniques in vitro, Transfection.
English descriptors
- KwdEn :
- ADAM Proteins (metabolism), ADAMTS Proteins, Adenoviridae (genetics), Animals, Calcium-Binding Proteins (genetics), Calcium-Binding Proteins (metabolism), Cells, Cultured, Endothelium, Vascular (cytology), Endothelium, Vascular (metabolism), HEK293 Cells, Humans, In Vitro Techniques, Lymphangiogenesis (physiology), Male, Mice, Mice, Inbred Strains, Models, Animal, Muscle, Skeletal (blood supply), Muscle, Skeletal (metabolism), Neovascularization, Physiologic (physiology), Procollagen N-Endopeptidase (metabolism), Transfection, Tumor Suppressor Proteins (genetics), Tumor Suppressor Proteins (metabolism), Vascular Endothelial Growth Factor C (metabolism), Vascular Endothelial Growth Factor Receptor-3 (metabolism).
- MESH :
- chemical , genetics : Calcium-Binding Proteins, Tumor Suppressor Proteins.
- chemical , metabolism : ADAM Proteins, Calcium-Binding Proteins, Procollagen N-Endopeptidase, Tumor Suppressor Proteins, Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor Receptor-3.
- chemical : ADAMTS Proteins.
- blood supply : Muscle, Skeletal.
- cytology : Endothelium, Vascular.
- genetics : Adenoviridae.
- metabolism : Endothelium, Vascular, Muscle, Skeletal.
- physiology : Lymphangiogenesis, Neovascularization, Physiologic.
- Animals, Cells, Cultured, HEK293 Cells, Humans, In Vitro Techniques, Male, Mice, Mice, Inbred Strains, Models, Animal, Transfection.
Abstract
Hennekam lymphangiectasia-lymphedema syndrome (Online Mendelian Inheritance in Man 235510) is a rare autosomal recessive disease, which is associated with mutations in the CCBE1 gene. Because of the striking phenotypic similarity of embryos lacking either the Ccbe1 gene or the lymphangiogenic growth factor Vegfc gene, we searched for collagen- and calcium-binding epidermal growth factor domains 1 (CCBE1) interactions with the vascular endothelial growth factor-C (VEGF-C) growth factor signaling pathway, which is critical in embryonic and adult lymphangiogenesis.
DOI: 10.1161/CIRCULATIONAHA.113.002779
PubMed: 24552833
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pubmed:24552833Le document en format XML
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<term>ADAMTS Proteins</term>
<term>Adenoviridae (genetics)</term>
<term>Animals</term>
<term>Calcium-Binding Proteins (genetics)</term>
<term>Calcium-Binding Proteins (metabolism)</term>
<term>Cells, Cultured</term>
<term>Endothelium, Vascular (cytology)</term>
<term>Endothelium, Vascular (metabolism)</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>In Vitro Techniques</term>
<term>Lymphangiogenesis (physiology)</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred Strains</term>
<term>Models, Animal</term>
<term>Muscle, Skeletal (blood supply)</term>
<term>Muscle, Skeletal (metabolism)</term>
<term>Neovascularization, Physiologic (physiology)</term>
<term>Procollagen N-Endopeptidase (metabolism)</term>
<term>Transfection</term>
<term>Tumor Suppressor Proteins (genetics)</term>
<term>Tumor Suppressor Proteins (metabolism)</term>
<term>Vascular Endothelial Growth Factor C (metabolism)</term>
<term>Vascular Endothelial Growth Factor Receptor-3 (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adenoviridae (génétique)</term>
<term>Animaux</term>
<term>Cellules HEK293</term>
<term>Cellules cultivées</term>
<term>Endothélium vasculaire (cytologie)</term>
<term>Endothélium vasculaire (métabolisme)</term>
<term>Facteur de croissance endothéliale vasculaire de type C (métabolisme)</term>
<term>Humains</term>
<term>Lignées consanguines de souris</term>
<term>Lymphangiogenèse (physiologie)</term>
<term>Modèles animaux</term>
<term>Muscles squelettiques ()</term>
<term>Muscles squelettiques (métabolisme)</term>
<term>Mâle</term>
<term>Néovascularisation physiologique (physiologie)</term>
<term>Procollagen peptidase (métabolisme)</term>
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<term>Protéines ADAMTS</term>
<term>Protéines de liaison au calcium (génétique)</term>
<term>Protéines de liaison au calcium (métabolisme)</term>
<term>Protéines suppresseurs de tumeurs (génétique)</term>
<term>Protéines suppresseurs de tumeurs (métabolisme)</term>
<term>Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme)</term>
<term>Souris</term>
<term>Techniques in vitro</term>
<term>Transfection</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Calcium-Binding Proteins</term>
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<term>Procollagen N-Endopeptidase</term>
<term>Tumor Suppressor Proteins</term>
<term>Vascular Endothelial Growth Factor C</term>
<term>Vascular Endothelial Growth Factor Receptor-3</term>
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<keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Muscle, Skeletal</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Endothélium vasculaire</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelium, Vascular</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenoviridae</term>
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<term>Protéines de liaison au calcium</term>
<term>Protéines suppresseurs de tumeurs</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelium, Vascular</term>
<term>Muscle, Skeletal</term>
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<term>Facteur de croissance endothéliale vasculaire de type C</term>
<term>Muscles squelettiques</term>
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<term>Protéines de liaison au calcium</term>
<term>Protéines suppresseurs de tumeurs</term>
<term>Récepteur-3 au facteur croissance endothéliale vasculaire</term>
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<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Lymphangiogenèse</term>
<term>Néovascularisation physiologique</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymphangiogenesis</term>
<term>Neovascularization, Physiologic</term>
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<term>Cells, Cultured</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>In Vitro Techniques</term>
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<term>Mice</term>
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<term>Muscles squelettiques</term>
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<front><div type="abstract" xml:lang="en">Hennekam lymphangiectasia-lymphedema syndrome (Online Mendelian Inheritance in Man 235510) is a rare autosomal recessive disease, which is associated with mutations in the CCBE1 gene. Because of the striking phenotypic similarity of embryos lacking either the Ccbe1 gene or the lymphangiogenic growth factor Vegfc gene, we searched for collagen- and calcium-binding epidermal growth factor domains 1 (CCBE1) interactions with the vascular endothelial growth factor-C (VEGF-C) growth factor signaling pathway, which is critical in embryonic and adult lymphangiogenesis.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24552833</PMID>
<DateCreated><Year>2014</Year>
<Month>05</Month>
<Day>13</Day>
</DateCreated>
<DateCompleted><Year>2014</Year>
<Month>10</Month>
<Day>01</Day>
</DateCompleted>
<DateRevised><Year>2016</Year>
<Month>11</Month>
<Day>25</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1524-4539</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>129</Volume>
<Issue>19</Issue>
<PubDate><Year>2014</Year>
<Month>May</Month>
<Day>13</Day>
</PubDate>
</JournalIssue>
<Title>Circulation</Title>
<ISOAbbreviation>Circulation</ISOAbbreviation>
</Journal>
<ArticleTitle>CCBE1 enhances lymphangiogenesis via A disintegrin and metalloprotease with thrombospondin motifs-3-mediated vascular endothelial growth factor-C activation.</ArticleTitle>
<Pagination><MedlinePgn>1962-71</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1161/CIRCULATIONAHA.113.002779</ELocationID>
<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Hennekam lymphangiectasia-lymphedema syndrome (Online Mendelian Inheritance in Man 235510) is a rare autosomal recessive disease, which is associated with mutations in the CCBE1 gene. Because of the striking phenotypic similarity of embryos lacking either the Ccbe1 gene or the lymphangiogenic growth factor Vegfc gene, we searched for collagen- and calcium-binding epidermal growth factor domains 1 (CCBE1) interactions with the vascular endothelial growth factor-C (VEGF-C) growth factor signaling pathway, which is critical in embryonic and adult lymphangiogenesis.</AbstractText>
<AbstractText Label="METHODS AND RESULTS" NlmCategory="RESULTS">By analyzing VEGF-C produced by CCBE1-transfected cells, we found that, whereas CCBE1 itself does not process VEGF-C, it promotes proteolytic cleavage of the otherwise poorly active 29/31-kDa form of VEGF-C by the A disintegrin and metalloprotease with thrombospondin motifs-3 protease, resulting in the mature 21/23-kDa form of VEGF-C, which induces increased VEGF-C receptor signaling. Adeno-associated viral vector-mediated transduction of CCBE1 into mouse skeletal muscle enhanced lymphangiogenesis and angiogenesis induced by adeno-associated viral vector-VEGF-C.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">These results identify A disintegrin and metalloprotease with thrombospondin motifs-3 as a VEGF-C-activating protease and reveal a novel type of regulation of a vascular growth factor by a protein that enhances its proteolytic cleavage and activation. The results suggest that CCBE1 is a potential therapeutic tool for the modulation of lymphangiogenesis and angiogenesis in a variety of diseases that involve the lymphatic system, such as lymphedema or lymphatic metastasis.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jeltsch</LastName>
<ForeName>Michael</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Wihuri Research Institute (M.J., A.A., V.-M.L., R.K., K.A.), Translational Cancer Biology Program (M.J., S.K.J., D.T., A.A., T.H., K.A.), and Department of Biomedicine (M.J.), Biomedicum Helsinki, University of Helsinki, Helsinki, Finland; Biotechnology Programme, Spanish National Cancer Research Centre, Madrid, Spain (S.O.); Hubrecht Institute, Utrecht, The Netherlands (T.K.); and Helsinki University Central Hospital, Helsinki, Finland (K.A.).</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jha</LastName>
<ForeName>Sawan Kumar</ForeName>
<Initials>SK</Initials>
</Author>
<Author ValidYN="Y"><LastName>Tvorogov</LastName>
<ForeName>Denis</ForeName>
<Initials>D</Initials>
</Author>
<Author ValidYN="Y"><LastName>Anisimov</LastName>
<ForeName>Andrey</ForeName>
<Initials>A</Initials>
</Author>
<Author ValidYN="Y"><LastName>Leppänen</LastName>
<ForeName>Veli-Matti</ForeName>
<Initials>VM</Initials>
</Author>
<Author ValidYN="Y"><LastName>Holopainen</LastName>
<ForeName>Tanja</ForeName>
<Initials>T</Initials>
</Author>
<Author ValidYN="Y"><LastName>Kivelä</LastName>
<ForeName>Riikka</ForeName>
<Initials>R</Initials>
</Author>
<Author ValidYN="Y"><LastName>Ortega</LastName>
<ForeName>Sagrario</ForeName>
<Initials>S</Initials>
</Author>
<Author ValidYN="Y"><LastName>Kärpanen</LastName>
<ForeName>Terhi</ForeName>
<Initials>T</Initials>
</Author>
<Author ValidYN="Y"><LastName>Alitalo</LastName>
<ForeName>Kari</ForeName>
<Initials>K</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>2014</Year>
<Month>02</Month>
<Day>19</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Circulation</MedlineTA>
<NlmUniqueID>0147763</NlmUniqueID>
<ISSNLinking>0009-7322</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C546964">CCBE1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D002135">Calcium-Binding Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D025521">Tumor Suppressor Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D042582">Vascular Endothelial Growth Factor C</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
<NameOfSubstance UI="C581309">FLT4 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
<NameOfSubstance UI="D040321">Vascular Endothelial Growth Factor Receptor-3</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.24.-</RegistryNumber>
<NameOfSubstance UI="D051722">ADAM Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.24.-</RegistryNumber>
<NameOfSubstance UI="D000071096">ADAMTS Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.24.-</RegistryNumber>
<NameOfSubstance UI="C434951">ADAMTS3 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.24.14</RegistryNumber>
<NameOfSubstance UI="D011348">Procollagen N-Endopeptidase</NameOfSubstance>
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<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
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<MeshHeading><DescriptorName UI="D004730" MajorTopicYN="N">Endothelium, Vascular</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D057809" MajorTopicYN="N">HEK293 Cells</DescriptorName>
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<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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