Signalling via vascular endothelial growth factor receptor-3 is sufficient for lymphangiogenesis in transgenic mice
Identifieur interne : 001750 ( Pmc/Curation ); précédent : 001749; suivant : 001751Signalling via vascular endothelial growth factor receptor-3 is sufficient for lymphangiogenesis in transgenic mice
Auteurs : Tanja Veikkola ; Lotta Jussila ; Taija Makinen ; Terhi Karpanen ; Michael Jeltsch ; Tatiana V. Petrova ; Hajime Kubo ; Gavin Thurston ; Donald M. Mcdonald ; Marc G. Achen ; Steven A. Stacker ; Kari AlitaloSource :
- The EMBO Journal [ 0261-4189 ] ; 2001.
Abstract
Vascular endothelial growth factor receptor-3 (VEGFR-3) has an essential role in the development of embryonic blood vessels; however, after midgestation its expression becomes restricted mainly to the developing lymphatic vessels. The VEGFR-3 ligand VEGF-C stimulates lymphangiogenesis in transgenic mice and in chick chorioallantoic membrane. As VEGF-C also binds VEGFR-2, which is expressed in lymphatic endothelia, it is not clear which receptors are responsible for the lymphangiogenic effects of VEGF-C. VEGF-D, which binds to the same receptors, has been reported to induce angiogenesis, but its lymphangiogenic potential is not known. In order to define the lymphangiogenic signalling pathway we have created transgenic mice overexpressing a VEGFR-3-specific mutant of VEGF-C (VEGF-C156S) or VEGF-D in epidermal keratinocytes under the keratin 14 promoter. Both transgenes induced the growth of lymphatic vessels in the skin, whereas the blood vessel architecture was not affected. Evidence was also obtained that these growth factors act in a paracrine manner
Url:
DOI: 10.1093/emboj/20.6.1223
PubMed: 11250889
PubMed Central: 145532
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Petrova</name></author><author><name sortKey="Kubo, Hajime" sort="Kubo, Hajime" uniqKey="Kubo H" first="Hajime" last="Kubo">Hajime Kubo</name></author><author><name sortKey="Thurston, Gavin" sort="Thurston, Gavin" uniqKey="Thurston G" first="Gavin" last="Thurston">Gavin Thurston</name><affiliation><nlm:aff id="N0x8b85658.0x9e207a8"></nlm:aff></affiliation></author><author><name sortKey="Mcdonald, Donald M" sort="Mcdonald, Donald M" uniqKey="Mcdonald D" first="Donald M." last="Mcdonald">Donald M. Mcdonald</name><affiliation><nlm:aff id="N0x8b85658.0x9e207a8"></nlm:aff></affiliation></author><author><name sortKey="Achen, Marc G" sort="Achen, Marc G" uniqKey="Achen M" first="Marc G." last="Achen">Marc G. Achen</name><affiliation><nlm:aff id="N0x8b85658.0x9e207a8"></nlm:aff></affiliation></author><author><name sortKey="Stacker, Steven A" sort="Stacker, Steven A" uniqKey="Stacker S" first="Steven A." last="Stacker">Steven A. 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Petrova</name></author><author><name sortKey="Kubo, Hajime" sort="Kubo, Hajime" uniqKey="Kubo H" first="Hajime" last="Kubo">Hajime Kubo</name></author><author><name sortKey="Thurston, Gavin" sort="Thurston, Gavin" uniqKey="Thurston G" first="Gavin" last="Thurston">Gavin Thurston</name><affiliation><nlm:aff id="N0x8b85658.0x9e207a8"></nlm:aff></affiliation></author><author><name sortKey="Mcdonald, Donald M" sort="Mcdonald, Donald M" uniqKey="Mcdonald D" first="Donald M." last="Mcdonald">Donald M. Mcdonald</name><affiliation><nlm:aff id="N0x8b85658.0x9e207a8"></nlm:aff></affiliation></author><author><name sortKey="Achen, Marc G" sort="Achen, Marc G" uniqKey="Achen M" first="Marc G." last="Achen">Marc G. Achen</name><affiliation><nlm:aff id="N0x8b85658.0x9e207a8"></nlm:aff></affiliation></author><author><name sortKey="Stacker, Steven A" sort="Stacker, Steven A" uniqKey="Stacker S" first="Steven A." last="Stacker">Steven A. Stacker</name><affiliation><nlm:aff id="N0x8b85658.0x9e207a8"></nlm:aff></affiliation></author><author><name sortKey="Alitalo, Kari" sort="Alitalo, Kari" uniqKey="Alitalo K" first="Kari" last="Alitalo">Kari Alitalo</name><affiliation><nlm:aff id="N0x8b85658.0x9e207a8"></nlm:aff></affiliation></author></analytic><series><title level="j">The EMBO Journal</title><idno type="ISSN">0261-4189</idno><idno type="eISSN">1460-2075</idno><imprint><date when="2001">2001</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Vascular endothelial growth factor receptor-3 (VEGFR-3) has an essential role in the development of embryonic blood vessels; however, after midgestation its expression becomes restricted mainly to the developing lymphatic vessels. The VEGFR-3 ligand VEGF-C stimulates lymphangiogenesis in transgenic mice and in chick chorioallantoic membrane. As VEGF-C also binds VEGFR-2, which is expressed in lymphatic endothelia, it is not clear which receptors are responsible for the lymphangiogenic effects of VEGF-C. VEGF-D, which binds to the same receptors, has been reported to induce angiogenesis, but its lymphangiogenic potential is not known. In order to define the lymphangiogenic signalling pathway we have created transgenic mice overexpressing a VEGFR-3-specific mutant of VEGF-C (VEGF-C156S) or VEGF-D in epidermal keratinocytes under the keratin 14 promoter. Both transgenes induced the growth of lymphatic vessels in the skin, whereas the blood vessel architecture was not affected. Evidence was also obtained that these growth factors act in a paracrine manner <italic>in vivo</italic>. These results demonstrate that stimulation of the VEGFR-3 signal transduction pathway is sufficient to induce specifically lymphangiogenesis <italic>in vivo</italic>.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">EMBO J</journal-id><journal-title>The EMBO Journal</journal-title><issn pub-type="ppub">0261-4189</issn><issn pub-type="epub">1460-2075</issn><publisher><publisher-name>Oxford University Press</publisher-name><publisher-loc>Oxford, UK</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">11250889</article-id><article-id pub-id-type="pmc">145532</article-id><article-id pub-id-type="publisher-id">cde137</article-id><article-id pub-id-type="doi">10.1093/emboj/20.6.1223</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Signalling via vascular endothelial growth factor receptor-3 is sufficient for lymphangiogenesis in transgenic mice</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Veikkola</surname><given-names>Tanja</given-names></name></contrib><contrib contrib-type="author"><name><surname>Jussila</surname><given-names>Lotta</given-names></name></contrib><contrib contrib-type="author"><name><surname>Makinen</surname><given-names>Taija</given-names></name></contrib><contrib contrib-type="author"><name><surname>Karpanen</surname><given-names>Terhi</given-names></name></contrib><contrib contrib-type="author"><name><surname>Jeltsch</surname><given-names>Michael</given-names></name></contrib><contrib contrib-type="author"><name><surname>Petrova</surname><given-names>Tatiana V.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Kubo</surname><given-names>Hajime</given-names></name></contrib><contrib contrib-type="author"><name><surname>Thurston</surname><given-names>Gavin</given-names></name><xref ref-type="aff" rid="N0x8b85658.0x9e207a8">1</xref></contrib><contrib contrib-type="author"><name><surname>McDonald</surname><given-names>Donald M.</given-names></name><xref ref-type="aff" rid="N0x8b85658.0x9e207a8">1</xref></contrib><contrib contrib-type="author"><name><surname>Achen</surname><given-names>Marc G.</given-names></name><xref ref-type="aff" rid="N0x8b85658.0x9e207a8">2</xref></contrib><contrib contrib-type="author"><name><surname>Stacker</surname><given-names>Steven A.</given-names></name><xref ref-type="aff" rid="N0x8b85658.0x9e207a8">2</xref></contrib><contrib contrib-type="author"><name><surname>Alitalo</surname><given-names>Kari</given-names></name><xref ref-type="aff" rid="N0x8b85658.0x9e207a8">3</xref></contrib></contrib-group><aff id="N0x8b85658.0x9e207a8">Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Haartman Institute, University of Helsinki, PO Box 21 (Haartmaninkatu 3), 00014 Helsinki, Finland,<label>1</label>Department of Anatomy and Cardiovascular Research Institute, University of California, San Francisco, CA 94143, USA and<label>2</label>Ludwig Institute for Cancer Research, PO Box 2008, Royal Melbourne Hospital, Parkville, Victoria 3050, Australia<label>3</label>Corresponding author e-mail:<email>Kari.Alitalo@helsinki.fi</email>T.Veikkola and L.Jussila contributed equally to this work</aff><pub-date pub-type="ppub"><day>15</day><month>3</month><year>2001</year></pub-date><volume>20</volume><issue>6</issue><fpage>1223</fpage><lpage>1231</lpage><ext-link ext-link-type="uri" xlink:href="http://www.emboj.oupjournals.org/content/vol20/issue6/"></ext-link><history><date date-type="received"><day>13</day><month>10</month><year>2000</year></date><date date-type="rev-recd"><day>20</day><month>12</month><year>2000</year></date><date date-type="accepted"><day>29</day><month>1</month><year>2001</year></date></history><copyright-statement>Copyright © 2001 European Molecular Biology Organization</copyright-statement><copyright-year>2001</copyright-year><abstract><p>Vascular endothelial growth factor receptor-3 (VEGFR-3) has an essential role in the development of embryonic blood vessels; however, after midgestation its expression becomes restricted mainly to the developing lymphatic vessels. The VEGFR-3 ligand VEGF-C stimulates lymphangiogenesis in transgenic mice and in chick chorioallantoic membrane. As VEGF-C also binds VEGFR-2, which is expressed in lymphatic endothelia, it is not clear which receptors are responsible for the lymphangiogenic effects of VEGF-C. VEGF-D, which binds to the same receptors, has been reported to induce angiogenesis, but its lymphangiogenic potential is not known. In order to define the lymphangiogenic signalling pathway we have created transgenic mice overexpressing a VEGFR-3-specific mutant of VEGF-C (VEGF-C156S) or VEGF-D in epidermal keratinocytes under the keratin 14 promoter. Both transgenes induced the growth of lymphatic vessels in the skin, whereas the blood vessel architecture was not affected. Evidence was also obtained that these growth factors act in a paracrine manner <italic>in vivo</italic>. These results demonstrate that stimulation of the VEGFR-3 signal transduction pathway is sufficient to induce specifically lymphangiogenesis <italic>in vivo</italic>.</p></abstract><kwd-group><kwd>angiogenesis/lymphangiogenesis/vascular endothelial growth factors (VEGFs)/VEGF receptors</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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