Phosphorylation of Akt and ERK1/2 Is Required for VEGF-A/VEGFR2-Induced Proliferation and Migration of Lymphatic Endothelium
Identifieur interne : 004C58 ( Main/Exploration ); précédent : 004C57; suivant : 004C59Phosphorylation of Akt and ERK1/2 Is Required for VEGF-A/VEGFR2-Induced Proliferation and Migration of Lymphatic Endothelium
Auteurs : Michael T. Dellinger [États-Unis] ; Rolf A. Brekken [États-Unis]Source :
- PLoS ONE [ 1932-6203 ] ; 2011.
Abstract
There is growing evidence that vascular endothelial growth factor-A (VEGF-A), a ligand of the receptor tyrosine kinases VEGFR1 and VEGFR2, promotes lymphangiogenesis. However, the underlying mechanisms by which VEGF-A induces the growth of lymphatic vessels remain poorly defined. Here we report that VEGFR2, not VEGFR1, is the primary receptor regulating VEGF-A-induced lymphangiogenesis. We show that specific inhibition of VEGF-A/VEGFR2 signaling with the fully human monoclonal antibody r84 significantly inhibits lymphangiogenesis in MDA-MB-231 tumors.
Url:
DOI: 10.1371/journal.pone.0028947
PubMed: 22174934
PubMed Central: 3236226
Affiliations:
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Dellinger</name><affiliation wicri:level="2"><nlm:aff id="aff1"><addr-line>Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation><affiliation wicri:level="2"><nlm:aff id="aff2"><addr-line>Hamon Center for Therapeutic Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Hamon Center for Therapeutic Oncology, University of Texas Southwestern Medical Center, Dallas, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Brekken, Rolf A" sort="Brekken, Rolf A" uniqKey="Brekken R" first="Rolf A." last="Brekken">Rolf A. Brekken</name><affiliation wicri:level="2"><nlm:aff id="aff1"><addr-line>Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation><affiliation wicri:level="2"><nlm:aff id="aff2"><addr-line>Hamon Center for Therapeutic Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Hamon Center for Therapeutic Oncology, University of Texas Southwestern Medical Center, Dallas, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation><affiliation wicri:level="2"><nlm:aff id="aff3"><addr-line>Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>There is growing evidence that vascular endothelial growth factor-A (VEGF-A), a ligand of the receptor tyrosine kinases VEGFR1 and VEGFR2, promotes lymphangiogenesis. However, the underlying mechanisms by which VEGF-A induces the growth of lymphatic vessels remain poorly defined. Here we report that VEGFR2, not VEGFR1, is the primary receptor regulating VEGF-A-induced lymphangiogenesis. We show that specific inhibition of VEGF-A/VEGFR2 signaling with the fully human monoclonal antibody r84 significantly inhibits lymphangiogenesis in MDA-MB-231 tumors. <italic>In vitro</italic> experiments with primary human dermal lymphatic endothelial cells (LECs) demonstrate that blocking VEGF-A activation of VEGFR2, not VEGFR1, significantly inhibits VEGF-A-induced proliferation and migration of LECs. We show that VEGF-A stimulation of LECs leads to the phosphorylation of VEGFR2 (Tyr 951, 1054, 1059, 1175, and 1214) which subsequently triggers PKC dependent phosphorylation of ERK1/2 and PI3-K dependent phosphorylation of Akt. Additionally, we demonstrate that inhibitors that suppress the phosphorylation of ERK1/2 and Akt significantly block VEGF-A- induced proliferation and migration of LECs. Together, these results shed light on the mechanisms regulating VEGF-A-induced proliferation and migration of LECs, reveal that VEGFR2 is the primary signaling VEGF-A receptor on lymphatic endothelium, and suggest that therapeutic agents targeting the VEGF-A/VEGFR2 axis could be useful in blocking the pathological formation of lymphatic vessels.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Witte, Mh" uniqKey="Witte M">MH Witte</name></author><author><name sortKey="Way, Dl" uniqKey="Way D">DL Way</name></author><author><name sortKey="Witte, Cl" uniqKey="Witte C">CL Witte</name></author><author><name sortKey="Bernas, M" uniqKey="Bernas M">M Bernas</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tammela, T" uniqKey="Tammela T">T Tammela</name></author><author><name sortKey="Alitalo, K" uniqKey="Alitalo K">K Alitalo</name></author></analytic></biblStruct><biblStruct><analytic><author><name 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Huot</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Makinen, T" uniqKey="Makinen T">T Makinen</name></author><author><name sortKey="Veikkola, T" uniqKey="Veikkola T">T Veikkola</name></author><author><name sortKey="Mustjoki, S" uniqKey="Mustjoki S">S Mustjoki</name></author><author><name sortKey="Karpanen, T" uniqKey="Karpanen T">T Karpanen</name></author><author><name sortKey="Catimel, B" uniqKey="Catimel B">B Catimel</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fulton, D" uniqKey="Fulton D">D Fulton</name></author><author><name sortKey="Gratton, Jp" uniqKey="Gratton J">JP Gratton</name></author><author><name sortKey="Mccabe, Tj" uniqKey="Mccabe T">TJ McCabe</name></author><author><name sortKey="Fontana, J" uniqKey="Fontana J">J Fontana</name></author><author><name sortKey="Fujio, Y" uniqKey="Fujio Y">Y Fujio</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Morales Ruiz, M" uniqKey="Morales Ruiz M">M Morales-Ruiz</name></author><author><name sortKey="Fulton, D" uniqKey="Fulton D">D Fulton</name></author><author><name sortKey="Sowa, G" uniqKey="Sowa G">G Sowa</name></author><author><name sortKey="Languino, Lr" uniqKey="Languino L">LR Languino</name></author><author><name sortKey="Fujio, Y" uniqKey="Fujio Y">Y Fujio</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lahdenranta, J" uniqKey="Lahdenranta J">J Lahdenranta</name></author><author><name sortKey="Hagendoorn, J" uniqKey="Hagendoorn J">J Hagendoorn</name></author><author><name sortKey="Padera, Tp" uniqKey="Padera T">TP Padera</name></author><author><name sortKey="Hoshida, T" uniqKey="Hoshida T">T Hoshida</name></author><author><name sortKey="Nelson, G" uniqKey="Nelson G">G Nelson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kajiya, K" uniqKey="Kajiya K">K Kajiya</name></author><author><name sortKey="Huggenberger, R" uniqKey="Huggenberger R">R Huggenberger</name></author><author><name sortKey="Drinnenberg, I" uniqKey="Drinnenberg I">I Drinnenberg</name></author><author><name sortKey="Ma, B" uniqKey="Ma B">B Ma</name></author><author><name sortKey="Detmar, M" uniqKey="Detmar M">M Detmar</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ran, S" uniqKey="Ran S">S Ran</name></author><author><name sortKey="Huang, X" uniqKey="Huang X">X Huang</name></author><author><name sortKey="Downes, A" uniqKey="Downes A">A Downes</name></author><author><name sortKey="Thorpe, Pe" uniqKey="Thorpe P">PE Thorpe</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Matsumoto, T" uniqKey="Matsumoto T">T Matsumoto</name></author><author><name sortKey="Claesson Welsh, L" uniqKey="Claesson Welsh L">L Claesson-Welsh</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Texas</li></region></list><tree><country name="États-Unis"><region name="Texas"><name sortKey="Dellinger, Michael T" sort="Dellinger, Michael T" uniqKey="Dellinger M" first="Michael T." last="Dellinger">Michael T. Dellinger</name></region><name sortKey="Brekken, Rolf A" sort="Brekken, Rolf A" uniqKey="Brekken R" first="Rolf A." last="Brekken">Rolf A. Brekken</name><name sortKey="Brekken, Rolf A" sort="Brekken, Rolf A" uniqKey="Brekken R" first="Rolf A." last="Brekken">Rolf A. Brekken</name><name sortKey="Brekken, Rolf A" sort="Brekken, Rolf A" uniqKey="Brekken R" first="Rolf A." last="Brekken">Rolf A. Brekken</name><name sortKey="Dellinger, Michael T" sort="Dellinger, Michael T" uniqKey="Dellinger M" first="Michael T." last="Dellinger">Michael T. Dellinger</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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