Adenoviral VEGF-C overexpression induces blood vessel enlargement, tortuosity, and leakiness but no sprouting angiogenesis in the skin or mucous membranes.
Identifieur interne : 004538 ( PubMed/Corpus ); précédent : 004537; suivant : 004539Adenoviral VEGF-C overexpression induces blood vessel enlargement, tortuosity, and leakiness but no sprouting angiogenesis in the skin or mucous membranes.
Auteurs : Anne Saaristo ; Tanja Veikkola ; Berndt Enholm ; Maija Hytönen ; Johanna Arola ; Katri Pajusola ; Païvi Turunen ; Michael Jeltsch ; Marika J. Karkkainen ; Dontscho Kerjaschki ; Hansruedi Bueler ; Seppo Yl Herttuala ; Kari AlitaloSource :
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology [ 1530-6860 ] ; 2002.
English descriptors
- KwdEn :
- Adenoviridae (genetics), Angiopoietin-1, Animals, Blood Vessels (anatomy & histology), Blood Vessels (metabolism), Capillary Permeability (drug effects), Cell Line, Dependovirus (genetics), Endothelial Growth Factors (genetics), Endothelial Growth Factors (metabolism), Genetic Vectors, Lymphatic System (growth & development), Lymphokines (genetics), Membrane Glycoproteins (pharmacology), Mice, Mice, Nude, Nasal Mucosa (blood supply), Neovascularization, Physiologic, Receptor Protein-Tyrosine Kinases (metabolism), Receptors, Growth Factor (metabolism), Receptors, Vascular Endothelial Growth Factor, Skin (blood supply), Skin (metabolism), Transfection, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factors.
- MESH :
- chemical , genetics : Endothelial Growth Factors, Lymphokines.
- chemical , metabolism : Endothelial Growth Factors, Receptor Protein-Tyrosine Kinases, Receptors, Growth Factor.
- chemical , pharmacology : Membrane Glycoproteins.
- chemical : Angiopoietin-1, Receptors, Vascular Endothelial Growth Factor, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factors.
- anatomy & histology : Blood Vessels.
- blood supply : Nasal Mucosa, Skin.
- drug effects : Capillary Permeability.
- genetics : Adenoviridae, Dependovirus.
- growth & development : Lymphatic System.
- metabolism : Blood Vessels, Skin.
- Animals, Cell Line, Genetic Vectors, Mice, Mice, Nude, Neovascularization, Physiologic, Transfection.
Abstract
Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are important regulators of blood and lymphatic vessel growth and vascular permeability. The VEGF-C/VEGFR-3 signaling pathway is crucial for lymphangiogenesis, and heterozygous inactivating missense mutations of the VEGFR-3 gene are associated with hereditary lymphedema. However, VEGF-C can have potent effects on blood vessels because its receptor VEGFR-3 is expressed in certain blood vessels and because the fully processed form of VEGF-C also binds to the VEGFR-2 of blood vessels. To characterize the in vivo effects of VEGF-C on blood and lymphatic vessels, we have overexpressed VEGF-C via adenovirus- and adeno-associated virus-mediated transfection in the skin and respiratory tract of athymic nude mice. This resulted in dose-dependent enlargement and tortuosity of veins, which, along with the collecting lymphatic vessels were found to express VEGFR-2. Expression of angiopoietin 1 blocked the increased leakiness of the blood vessels induced by VEGF-C whereas vessel enlargement and lymphangiogenesis were not affected. However, angiogenic sprouting of new blood vessels was not observed in response to AdVEGF-C or AAV-VEGF-C. These results show that virally produced VEGF-C induces blood vessel changes, including vascular leak, but its angiogenic potency is much reduced compared with VEGF in normal skin.
DOI: 10.1096/fj.01-1042com
PubMed: 12087065
Links to Exploration step
pubmed:12087065Le document en format XML
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Karkkainen</name></author><author><name sortKey="Kerjaschki, Dontscho" sort="Kerjaschki, Dontscho" uniqKey="Kerjaschki D" first="Dontscho" last="Kerjaschki">Dontscho Kerjaschki</name></author><author><name sortKey="Bueler, Hansruedi" sort="Bueler, Hansruedi" uniqKey="Bueler H" first="Hansruedi" last="Bueler">Hansruedi Bueler</name></author><author><name sortKey="Yl Herttuala, Seppo" sort="Yl Herttuala, Seppo" uniqKey="Yl Herttuala S" first="Seppo" last="Yl Herttuala">Seppo Yl Herttuala</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">FASEB journal : official publication of the Federation of American Societies for Experimental Biology</title><idno type="eISSN">1530-6860</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenoviridae (genetics)</term><term>Angiopoietin-1</term><term>Animals</term><term>Blood Vessels (anatomy & histology)</term><term>Blood Vessels (metabolism)</term><term>Capillary Permeability (drug effects)</term><term>Cell Line</term><term>Dependovirus (genetics)</term><term>Endothelial Growth Factors (genetics)</term><term>Endothelial Growth Factors (metabolism)</term><term>Genetic Vectors</term><term>Lymphatic System (growth & development)</term><term>Lymphokines (genetics)</term><term>Membrane Glycoproteins (pharmacology)</term><term>Mice</term><term>Mice, Nude</term><term>Nasal Mucosa (blood supply)</term><term>Neovascularization, Physiologic</term><term>Receptor Protein-Tyrosine Kinases (metabolism)</term><term>Receptors, Growth Factor (metabolism)</term><term>Receptors, Vascular Endothelial Growth Factor</term><term>Skin (blood supply)</term><term>Skin (metabolism)</term><term>Transfection</term><term>Vascular Endothelial Growth Factor A</term><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Endothelial Growth Factors</term><term>Lymphokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Endothelial Growth Factors</term><term>Receptor Protein-Tyrosine Kinases</term><term>Receptors, Growth Factor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Membrane Glycoproteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Angiopoietin-1</term><term>Receptors, Vascular Endothelial Growth Factor</term><term>Vascular Endothelial Growth Factor A</term><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factors</term></keywords><keywords scheme="MESH" qualifier="anatomy & histology" xml:lang="en"><term>Blood Vessels</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Nasal Mucosa</term><term>Skin</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Capillary Permeability</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenoviridae</term><term>Dependovirus</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Lymphatic System</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Blood Vessels</term><term>Skin</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Genetic Vectors</term><term>Mice</term><term>Mice, Nude</term><term>Neovascularization, Physiologic</term><term>Transfection</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are important regulators of blood and lymphatic vessel growth and vascular permeability. The VEGF-C/VEGFR-3 signaling pathway is crucial for lymphangiogenesis, and heterozygous inactivating missense mutations of the VEGFR-3 gene are associated with hereditary lymphedema. However, VEGF-C can have potent effects on blood vessels because its receptor VEGFR-3 is expressed in certain blood vessels and because the fully processed form of VEGF-C also binds to the VEGFR-2 of blood vessels. To characterize the in vivo effects of VEGF-C on blood and lymphatic vessels, we have overexpressed VEGF-C via adenovirus- and adeno-associated virus-mediated transfection in the skin and respiratory tract of athymic nude mice. This resulted in dose-dependent enlargement and tortuosity of veins, which, along with the collecting lymphatic vessels were found to express VEGFR-2. Expression of angiopoietin 1 blocked the increased leakiness of the blood vessels induced by VEGF-C whereas vessel enlargement and lymphangiogenesis were not affected. However, angiogenic sprouting of new blood vessels was not observed in response to AdVEGF-C or AAV-VEGF-C. These results show that virally produced VEGF-C induces blood vessel changes, including vascular leak, but its angiogenic potency is much reduced compared with VEGF in normal skin.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12087065</PMID><DateCreated><Year>2002</Year><Month>06</Month><Day>27</Day></DateCreated><DateCompleted><Year>2002</Year><Month>07</Month><Day>23</Day></DateCompleted><DateRevised><Year>2012</Year><Month>02</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1530-6860</ISSN><JournalIssue CitedMedium="Internet"><Volume>16</Volume><Issue>9</Issue><PubDate><Year>2002</Year><Month>Jul</Month></PubDate></JournalIssue><Title>FASEB journal : official publication of the Federation of American Societies for Experimental Biology</Title><ISOAbbreviation>FASEB J.</ISOAbbreviation></Journal><ArticleTitle>Adenoviral VEGF-C overexpression induces blood vessel enlargement, tortuosity, and leakiness but no sprouting angiogenesis in the skin or mucous membranes.</ArticleTitle><Pagination><MedlinePgn>1041-9</MedlinePgn></Pagination><Abstract><AbstractText>Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are important regulators of blood and lymphatic vessel growth and vascular permeability. The VEGF-C/VEGFR-3 signaling pathway is crucial for lymphangiogenesis, and heterozygous inactivating missense mutations of the VEGFR-3 gene are associated with hereditary lymphedema. However, VEGF-C can have potent effects on blood vessels because its receptor VEGFR-3 is expressed in certain blood vessels and because the fully processed form of VEGF-C also binds to the VEGFR-2 of blood vessels. To characterize the in vivo effects of VEGF-C on blood and lymphatic vessels, we have overexpressed VEGF-C via adenovirus- and adeno-associated virus-mediated transfection in the skin and respiratory tract of athymic nude mice. This resulted in dose-dependent enlargement and tortuosity of veins, which, along with the collecting lymphatic vessels were found to express VEGFR-2. Expression of angiopoietin 1 blocked the increased leakiness of the blood vessels induced by VEGF-C whereas vessel enlargement and lymphangiogenesis were not affected. However, angiogenic sprouting of new blood vessels was not observed in response to AdVEGF-C or AAV-VEGF-C. These results show that virally produced VEGF-C induces blood vessel changes, including vascular leak, but its angiogenic potency is much reduced compared with VEGF in normal skin.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Saaristo</LastName><ForeName>Anne</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum, University of Helsinki and Helsinki University Central Hospital, 00014 Helsinki, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Veikkola</LastName><ForeName>Tanja</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Enholm</LastName><ForeName>Berndt</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Hytönen</LastName><ForeName>Maija</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Arola</LastName><ForeName>Johanna</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Pajusola</LastName><ForeName>Katri</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Turunen</LastName><ForeName>Païvi</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Jeltsch</LastName><ForeName>Michael</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Karkkainen</LastName><ForeName>Marika J</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Kerjaschki</LastName><ForeName>Dontscho</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Bueler</LastName><ForeName>Hansruedi</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Ylä-Herttuala</LastName><ForeName>Seppo</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Alitalo</LastName><ForeName>Kari</ForeName><Initials>K</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>FASEB J</MedlineTA><NlmUniqueID>8804484</NlmUniqueID><ISSNLinking>0892-6638</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042683">Angiopoietin-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C467628">Angpt1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016228">Endothelial Growth Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008222">Lymphokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008562">Membrane Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017978">Receptors, Growth Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042461">Vascular Endothelial Growth Factor A</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042582">Vascular Endothelial Growth Factor C</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042442">Vascular Endothelial Growth Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D020794">Receptor Protein-Tyrosine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D040262">Receptors, Vascular Endothelial Growth Factor</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000256" MajorTopicYN="N">Adenoviridae</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042683" MajorTopicYN="N">Angiopoietin-1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001808" MajorTopicYN="N">Blood Vessels</DescriptorName><QualifierName UI="Q000033" MajorTopicYN="N">anatomy & histology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002199" MajorTopicYN="N">Capillary Permeability</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000229" MajorTopicYN="N">Dependovirus</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016228" MajorTopicYN="N">Endothelial Growth Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005822" MajorTopicYN="N">Genetic Vectors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008208" MajorTopicYN="N">Lymphatic System</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008222" MajorTopicYN="N">Lymphokines</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008562" MajorTopicYN="N">Membrane Glycoproteins</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009297" MajorTopicYN="N">Nasal Mucosa</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="N">blood supply</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018919" MajorTopicYN="Y">Neovascularization, Physiologic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020794" MajorTopicYN="N">Receptor Protein-Tyrosine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017978" MajorTopicYN="N">Receptors, Growth Factor</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D040262" MajorTopicYN="N">Receptors, Vascular Endothelial Growth Factor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012867" MajorTopicYN="N">Skin</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="Y">blood supply</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042461" MajorTopicYN="N">Vascular Endothelial Growth Factor A</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042582" MajorTopicYN="N">Vascular Endothelial Growth Factor C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042442" MajorTopicYN="N">Vascular Endothelial Growth Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>6</Month><Day>28</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>7</Month><Day>24</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>6</Month><Day>28</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12087065</ArticleId><ArticleId IdType="doi">10.1096/fj.01-1042com</ArticleId><ArticleId IdType="pii">16/9/1041</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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