Activated forms of VEGF-C and VEGF-D provide improved vascular function in skeletal muscle.
Identifieur interne : 002E66 ( PubMed/Corpus ); précédent : 002E65; suivant : 002E67Activated forms of VEGF-C and VEGF-D provide improved vascular function in skeletal muscle.
Auteurs : Andrey Anisimov ; Annamari Alitalo ; Petra Korpisalo ; Jarkko Soronen ; Seppo Kaijalainen ; Veli-Matti Lepp Nen ; Michael Jeltsch ; Seppo Yl Herttuala ; Kari AlitaloSource :
- Circulation research [ 1524-4571 ] ; 2009.
English descriptors
- KwdEn :
- Animals, Blood Vessels (physiology), Dimerization, Drug Stability, Heart (physiology), Humans, Lymphatic Vessels (physiology), Mice, Mice, Transgenic, Muscle, Skeletal (blood supply), Muscle, Skeletal (physiology), Mutation, Polymorphism, Single Nucleotide, Recombinant Proteins (metabolism), Vascular Endothelial Growth Factor B (genetics), Vascular Endothelial Growth Factor B (physiology), Vascular Endothelial Growth Factor C (genetics), Vascular Endothelial Growth Factor C (physiology), Vascular Endothelial Growth Factor Receptor-2 (physiology).
- MESH :
- chemical , genetics : Vascular Endothelial Growth Factor B, Vascular Endothelial Growth Factor C.
- chemical , metabolism : Recombinant Proteins.
- blood supply : Muscle, Skeletal.
- physiology : Blood Vessels, Heart, Lymphatic Vessels, Muscle, Skeletal, Vascular Endothelial Growth Factor B, Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor Receptor-2.
- Animals, Dimerization, Drug Stability, Humans, Mice, Mice, Transgenic, Mutation, Polymorphism, Single Nucleotide.
Abstract
The therapeutic potential of vascular endothelial growth factor (VEGF)-C and VEGF-D in skeletal muscle has been of considerable interest as these factors have both angiogenic and lymphangiogenic activities. Previous studies have mainly used adenoviral gene delivery for short-term expression of VEGF-C and VEGF-D in pig, rabbit, and mouse skeletal muscles. Here we have used the activated mature forms of VEGF-C and VEGF-D expressed via recombinant adeno-associated virus (rAAV), which provides stable, long-lasting transgene expression in various tissues including skeletal muscle. Mouse tibialis anterior muscle was transduced with rAAV encoding human or mouse VEGF-C or VEGF-D. Two weeks later, immunohistochemical analysis showed increased numbers of both blood and lymph vessels, and Doppler ultrasound analysis indicated increased blood vessel perfusion. The lymphatic vessels further increased at the 4-week time point were functional, as shown by FITC-lectin uptake and transport. Furthermore, receptor activation and arteriogenic activity were increased by an alanine substitution mutant of human VEGF-C (C137A) having an increased dimer stability and by a chimeric CAC growth factor that contained the VEGF receptor-binding domain flanked by VEGF-C propeptides, but only the latter promoted significantly more blood vessel perfusion when compared to the other growth factors studied. We conclude that long-term expression of VEGF-C and VEGF-D in skeletal muscle results in the generation of new functional blood and lymphatic vessels. The therapeutic value of intramuscular lymph vessels in draining tissue edema and lymphedema can now be evaluated using this model system.
DOI: 10.1161/CIRCRESAHA.109.197830
PubMed: 19443835
Links to Exploration step
pubmed:19443835Le document en format XML
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Soronen</name></author><author><name sortKey="Kaijalainen, Seppo" sort="Kaijalainen, Seppo" uniqKey="Kaijalainen S" first="Seppo" last="Kaijalainen">Seppo Kaijalainen</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="Jeltsch, Michael" sort="Jeltsch, Michael" uniqKey="Jeltsch M" first="Michael" last="Jeltsch">Michael Jeltsch</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></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19443835</idno><idno type="pmid">19443835</idno><idno 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Nucleotide</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The therapeutic potential of vascular endothelial growth factor (VEGF)-C and VEGF-D in skeletal muscle has been of considerable interest as these factors have both angiogenic and lymphangiogenic activities. Previous studies have mainly used adenoviral gene delivery for short-term expression of VEGF-C and VEGF-D in pig, rabbit, and mouse skeletal muscles. Here we have used the activated mature forms of VEGF-C and VEGF-D expressed via recombinant adeno-associated virus (rAAV), which provides stable, long-lasting transgene expression in various tissues including skeletal muscle. Mouse tibialis anterior muscle was transduced with rAAV encoding human or mouse VEGF-C or VEGF-D. Two weeks later, immunohistochemical analysis showed increased numbers of both blood and lymph vessels, and Doppler ultrasound analysis indicated increased blood vessel perfusion. The lymphatic vessels further increased at the 4-week time point were functional, as shown by FITC-lectin uptake and transport. Furthermore, receptor activation and arteriogenic activity were increased by an alanine substitution mutant of human VEGF-C (C137A) having an increased dimer stability and by a chimeric CAC growth factor that contained the VEGF receptor-binding domain flanked by VEGF-C propeptides, but only the latter promoted significantly more blood vessel perfusion when compared to the other growth factors studied. We conclude that long-term expression of VEGF-C and VEGF-D in skeletal muscle results in the generation of new functional blood and lymphatic vessels. The therapeutic value of intramuscular lymph vessels in draining tissue edema and lymphedema can now be evaluated using this model system.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19443835</PMID><DateCreated><Year>2009</Year><Month>06</Month><Day>05</Day></DateCreated><DateCompleted><Year>2009</Year><Month>07</Month><Day>08</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1524-4571</ISSN><JournalIssue CitedMedium="Internet"><Volume>104</Volume><Issue>11</Issue><PubDate><Year>2009</Year><Month>Jun</Month><Day>05</Day></PubDate></JournalIssue><Title>Circulation research</Title><ISOAbbreviation>Circ. Res.</ISOAbbreviation></Journal><ArticleTitle>Activated forms of VEGF-C and VEGF-D provide improved vascular function in skeletal muscle.</ArticleTitle><Pagination><MedlinePgn>1302-12</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1161/CIRCRESAHA.109.197830</ELocationID><Abstract><AbstractText>The therapeutic potential of vascular endothelial growth factor (VEGF)-C and VEGF-D in skeletal muscle has been of considerable interest as these factors have both angiogenic and lymphangiogenic activities. Previous studies have mainly used adenoviral gene delivery for short-term expression of VEGF-C and VEGF-D in pig, rabbit, and mouse skeletal muscles. Here we have used the activated mature forms of VEGF-C and VEGF-D expressed via recombinant adeno-associated virus (rAAV), which provides stable, long-lasting transgene expression in various tissues including skeletal muscle. Mouse tibialis anterior muscle was transduced with rAAV encoding human or mouse VEGF-C or VEGF-D. Two weeks later, immunohistochemical analysis showed increased numbers of both blood and lymph vessels, and Doppler ultrasound analysis indicated increased blood vessel perfusion. The lymphatic vessels further increased at the 4-week time point were functional, as shown by FITC-lectin uptake and transport. Furthermore, receptor activation and arteriogenic activity were increased by an alanine substitution mutant of human VEGF-C (C137A) having an increased dimer stability and by a chimeric CAC growth factor that contained the VEGF receptor-binding domain flanked by VEGF-C propeptides, but only the latter promoted significantly more blood vessel perfusion when compared to the other growth factors studied. We conclude that long-term expression of VEGF-C and VEGF-D in skeletal muscle results in the generation of new functional blood and lymphatic vessels. The therapeutic value of intramuscular lymph vessels in draining tissue edema and lymphedema can now be evaluated using this model system.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Anisimov</LastName><ForeName>Andrey</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Molecular/Cancer Biology Laboratory, Biomedicum Helsinki, Department of Pathology, Haartman Institute and Helsinki University Central Hospital, University of Helsinki, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alitalo</LastName><ForeName>Annamari</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Korpisalo</LastName><ForeName>Petra</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Soronen</LastName><ForeName>Jarkko</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Kaijalainen</LastName><ForeName>Seppo</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Leppänen</LastName><ForeName>Veli-Matti</ForeName><Initials>VM</Initials></Author><Author ValidYN="Y"><LastName>Jeltsch</LastName><ForeName>Michael</ForeName><Initials>M</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><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL075183</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL075183-02</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>5-R01-HL075183-02</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>05</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Circ Res</MedlineTA><NlmUniqueID>0047103</NlmUniqueID><ISSNLinking>0009-7330</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011994">Recombinant Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C467485">VEGFB protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C467486">VEGFC protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042561">Vascular Endothelial Growth Factor 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Version="1">19366703</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>EMBO J. 1997 Jul 1;16(13):3898-911</RefSource><PMID Version="1">9233800</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8657-62</RefSource><PMID Version="1">10411931</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cancer Cell. 2005 Jan;7(1):101-11</RefSource><PMID Version="1">15652753</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Blood. 2005 Feb 15;105(4):1424-30</RefSource><PMID Version="1">15507527</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Clin Sci (Lond). 2005 Sep;109(3):227-41</RefSource><PMID Version="1">16104843</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Angiogenesis. 2005;8(3):241-51</RefSource><PMID Version="1">16308736</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Bioinformatics. 2006 Jan 15;22(2):195-201</RefSource><PMID Version="1">16301204</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Mol Biol. 2006 May 26;359(1):76-85</RefSource><PMID Version="1">16616187</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2006 Jun 9;98(11):1373-80</RefSource><PMID Version="1">16690881</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 1999 Nov 5;274(45):32127-36</RefSource><PMID Version="1">10542248</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2000 May;14(7):871-6</RefSource><PMID Version="1">10783140</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2001 Apr 13;276(15):12153-61</RefSource><PMID Version="1">11069911</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2001 Jun 1;276(22):19166-71</RefSource><PMID Version="1">11279005</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Virol. 2001 Aug;75(15):6969-76</RefSource><PMID Version="1">11435577</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>EMBO J. 2001 Sep 3;20(17):4762-73</RefSource><PMID Version="1">11532940</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2002 Sep;161(3):947-56</RefSource><PMID Version="1">12213723</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2003 May 30;92(10):1098-106</RefSource><PMID Version="1">12714562</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Med. 2003 Jun;9(6):694-701</RefSource><PMID Version="1">12778168</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Gene Ther. 2003 Oct 10;14(15):1451-62</RefSource><PMID Version="1">14577925</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circulation. 2004 Mar 2;109(8):1029-35</RefSource><PMID Version="1">14967735</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Gene Med. 2004 May;6(5):545-54</RefSource><PMID Version="1">15133765</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem Biophys Res Commun. 2004 Nov 12;324(2):909-15</RefSource><PMID Version="1">15474514</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Divers. 2006 Nov;10(4):515-27</RefSource><PMID Version="1">16972015</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Histochem Cell Biol. 2007 Jan;127(1):31-40</RefSource><PMID Version="1">16924525</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cancer Res. 2007 Jan 15;67(2):593-9</RefSource><PMID Version="1">17234768</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Gene Ther. 2007 Mar;18(3):232-44</RefSource><PMID Version="1">17362136</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2007 May 25;100(10):1460-7</RefSource><PMID Version="1">17478734</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trends Immunol. 2007 Dec;28(12):519-24</RefSource><PMID Version="1">17981504</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Med. 2007 Dec;13(12):1458-66</RefSource><PMID Version="1">18059280</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cancer Res. 2008 Feb 15;68(4):1100-9</RefSource><PMID Version="1">18281485</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Annu Rev Pathol. 2008;3:367-97</RefSource><PMID Version="1">18039141</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arterioscler Thromb Vasc Biol. 2008 Apr;28(4):658-64</RefSource><PMID Version="1">18174461</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Contrib Nephrol. 2008;159:63-77</RefSource><PMID Version="1">18391585</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cardiovasc Res. 2008 May 1;78(2):315-23</RefSource><PMID Version="1">18065770</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2008 Jun;118(6):2062-75</RefSource><PMID Version="1">18483621</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Angiogenesis. 2008;11(2):109-19</RefSource><PMID Version="1">18293091</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Ther. 2008 Jul;16(7):1189-99</RefSource><PMID Version="1">18500252</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Rev Cancer. 2008 Aug;8(8):618-31</RefSource><PMID Version="1">18633355</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2008 Jul 31;454(7204):656-60</RefSource><PMID Version="1">18594512</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Protoc. 2008;3(11):1703-8</RefSource><PMID Version="1">18846097</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2008 Dec;173(6):1891-901</RefSource><PMID Version="1">18988807</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Ther. 2009 Jan;17(1):73-80</RefSource><PMID Version="1">18941441</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7192-7</RefSource><PMID Version="1">9207067</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001808" MajorTopicYN="N">Blood Vessels</DescriptorName><QualifierName UI="Q000502" 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IdType="pii">CIRCRESAHA.109.197830</ArticleId><ArticleId IdType="doi">10.1161/CIRCRESAHA.109.197830</ArticleId><ArticleId IdType="pmc">PMC2776655</ArticleId><ArticleId IdType="mid">NIHMS127228</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Activated forms of VEGF-C and VEGF-D provide improved vascular function in skeletal muscle.
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