CCBE1 enhances lymphangiogenesis via A disintegrin and metalloprotease with thrombospondin motifs-3-mediated vascular endothelial growth factor-C activation.
Identifieur interne : 001669 ( PubMed/Corpus ); 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 ; 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.
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
Links to Exploration step
pubmed:24552833Le document en format XML
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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.).</nlm:affiliation></affiliation></author><author><name sortKey="Jha, Sawan Kumar" sort="Jha, Sawan Kumar" uniqKey="Jha S" first="Sawan Kumar" last="Jha">Sawan Kumar Jha</name></author><author><name sortKey="Tvorogov, Denis" sort="Tvorogov, Denis" uniqKey="Tvorogov D" first="Denis" last="Tvorogov">Denis Tvorogov</name></author><author><name sortKey="Anisimov, Andrey" sort="Anisimov, Andrey" uniqKey="Anisimov A" first="Andrey" last="Anisimov">Andrey Anisimov</name></author><author><name sortKey="Lepp Nen, Veli Matti" sort="Lepp Nen, Veli Matti" uniqKey="Lepp Nen V" first="Veli-Matti" last="Lepp Nen">Veli-Matti Lepp Nen</name></author><author><name sortKey="Holopainen, Tanja" sort="Holopainen, Tanja" uniqKey="Holopainen T" first="Tanja" last="Holopainen">Tanja Holopainen</name></author><author><name sortKey="Kivel, Riikka" sort="Kivel, Riikka" uniqKey="Kivel R" first="Riikka" last="Kivel">Riikka Kivel</name></author><author><name sortKey="Ortega, Sagrario" sort="Ortega, Sagrario" uniqKey="Ortega S" first="Sagrario" last="Ortega">Sagrario Ortega</name></author><author><name sortKey="K Rpanen, Terhi" sort="K Rpanen, Terhi" uniqKey="K Rpanen T" first="Terhi" last="K Rpanen">Terhi K Rpanen</name></author><author><name sortKey="Alitalo, Kari" sort="Alitalo, Kari" uniqKey="Alitalo K" first="Kari" last="Alitalo">Kari Alitalo</name></author></analytic><series><title level="j">Circulation</title><idno type="eISSN">1524-4539</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>ADAM Proteins (metabolism)</term><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="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Calcium-Binding Proteins</term><term>Tumor Suppressor Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>ADAM Proteins</term><term>Calcium-Binding Proteins</term><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></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>ADAMTS Proteins</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelium, Vascular</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenoviridae</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelium, Vascular</term><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymphangiogenesis</term><term>Neovascularization, Physiologic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>HEK293 Cells</term><term>Humans</term><term>In Vitro Techniques</term><term>Male</term><term>Mice</term><term>Mice, Inbred Strains</term><term>Models, Animal</term><term>Transfection</term></keywords></textClass></profileDesc></teiHeader><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></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D051722" MajorTopicYN="N">ADAM Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071096" MajorTopicYN="N">ADAMTS Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000256" MajorTopicYN="N">Adenoviridae</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002135" MajorTopicYN="N">Calcium-Binding Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><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></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066298" MajorTopicYN="N">In Vitro Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008815" MajorTopicYN="N">Mice, Inbred Strains</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D023421" MajorTopicYN="N">Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018482" MajorTopicYN="N">Muscle, Skeletal</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="N">blood supply</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018919" MajorTopicYN="N">Neovascularization, Physiologic</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011348" MajorTopicYN="N">Procollagen N-Endopeptidase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D025521" MajorTopicYN="N">Tumor Suppressor Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042582" MajorTopicYN="N">Vascular Endothelial Growth Factor C</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D040321" MajorTopicYN="N">Vascular Endothelial Growth Factor Receptor-3</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">angiogenesis effect</Keyword><Keyword MajorTopicYN="N">endothelium</Keyword><Keyword MajorTopicYN="N">growth substances</Keyword><Keyword MajorTopicYN="N">metalloproteinases</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>2</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>2</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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