The lymphangiogenic growth factors VEGF-C and D are ligands for the integrin α9β1*
Identifieur interne : 003662 ( Pmc/Curation ); précédent : 003661; suivant : 003663The lymphangiogenic growth factors VEGF-C and D are ligands for the integrin α9β1*
Auteurs : Nicholas E. Vlahakis [États-Unis] ; Bradford A. Young ; Amha Atakilit ; Dean SheppardSource :
- The Journal of biological chemistry [ 0021-9258 ] ; 2004.
Abstract
Mice homozygous for a null mutation of the integrin α9 subunit die 6–12 days after birth from bilateral chylothoraces suggesting an underlying defect in lymphatic development. However, until now the mechanisms by which the integrin α9β1 modulates lymphangiogenesis have not been described. In this study we show that adhesion to and migration on the lymphangiogenic vascular endothelial growth factors (VEGF)-C and D are α9β1 dependent. Mouse embryonic fibroblasts and human colon carcinoma cells (SW-480) transfected to express α9β1 adhered and/or migrated on both growth factors in a concentration-dependent fashion, and both adhesion and migration were abrogated by anti-α9β1 function blocking antibody. In SW-480 cells, which lack cognate receptors for VEGFC and D, both growth factors induced α9β1-depedent Erk and paxillin phosphorylation. Human microvascular endothelial cells, which express both α9β1 and VEGF-R3, also adhered to and migrated on both growth factors, and both responses, were blocked by anti-α9β1 antibody. Furthermore, in a solid phase binding assay recombinant VEGF-C and D bound to purified α9β1 integrin in a dose- and cation-dependent fashion showing that VEGF-C and VEGF-D are ligands for the integrin α9β1. The interaction between α9β1 and VEGF-C and/or D may begin to explain the abnormal lymphatic phenotype of the α9 knockout mice.
Url:
DOI: 10.1074/jbc.M412816200
PubMed: 15590642
PubMed Central: 1368959
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Nicholas E. Vlahakis<affiliation><nlm:aff id="A1"> From the Lung Biology Center, University of California San Francisco, Box 2922, San Francisco, CA, 94143-2922</nlm:aff>
<wicri:noCountry code="subfield">94143-2922</wicri:noCountry>
</affiliation>
<affiliation wicri:level="2"><nlm:aff id="A2"> Thoracic Disease Research Unit, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Minnesota</region>
</placeName>
<wicri:cityArea> Thoracic Disease Research Unit, Mayo Clinic College of Medicine, 200 First St SW, Rochester</wicri:cityArea>
</affiliation>
<affiliation><nlm:aff id="A1"> From the Lung Biology Center, University of California San Francisco, Box 2922, San Francisco, CA, 94143-2922</nlm:aff>
<wicri:noCountry code="subfield">94143-2922</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A1"> From the Lung Biology Center, University of California San Francisco, Box 2922, San Francisco, CA, 94143-2922</nlm:aff>
<wicri:noCountry code="subfield">94143-2922</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A1"> From the Lung Biology Center, University of California San Francisco, Box 2922, San Francisco, CA, 94143-2922</nlm:aff>
<wicri:noCountry code="subfield">94143-2922</wicri:noCountry>
</affiliation>
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<series><title level="j">The Journal of biological chemistry</title>
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<front><div type="abstract" xml:lang="en"><title>Summary</title>
<p id="P2">Mice homozygous for a null mutation of the integrin α9 subunit die 6–12 days after birth from bilateral chylothoraces suggesting an underlying defect in lymphatic development. However, until now the mechanisms by which the integrin α9β1 modulates lymphangiogenesis have not been described. In this study we show that adhesion to and migration on the lymphangiogenic vascular endothelial growth factors (VEGF)-C and D are α9β1 dependent. Mouse embryonic fibroblasts and human colon carcinoma cells (SW-480) transfected to express α9β1 adhered and/or migrated on both growth factors in a concentration-dependent fashion, and both adhesion and migration were abrogated by anti-α9β1 function blocking antibody. In SW-480 cells, which lack cognate receptors for VEGFC and D, both growth factors induced α9β1-depedent Erk and paxillin phosphorylation. Human microvascular endothelial cells, which express both α9β1 and VEGF-R3, also adhered to and migrated on both growth factors, and both responses, were blocked by anti-α9β1 antibody. Furthermore, in a solid phase binding assay recombinant VEGF-C and D bound to purified α9β1 integrin in a dose- and cation-dependent fashion showing that VEGF-C and VEGF-D are ligands for the integrin α9β1. The interaction between α9β1 and VEGF-C and/or D may begin to explain the abnormal lymphatic phenotype of the α9 knockout mice.</p>
</div>
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<front><journal-meta><journal-id journal-id-type="nlm-journal-id">2985121R</journal-id>
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<journal-id journal-id-type="nlm-ta">J Biol Chem</journal-id>
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<title-group><article-title>The lymphangiogenic growth factors VEGF-C and D are ligands for the integrin α9β1<xref rid="FN2" ref-type="fn">*</xref>
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<contrib-group><contrib contrib-type="author"><name><surname>Vlahakis</surname>
<given-names>Nicholas E.</given-names>
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<xref rid="A1" ref-type="aff">¶</xref>
<xref rid="A2" ref-type="aff">‡</xref>
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<contrib contrib-type="author"><name><surname>Young</surname>
<given-names>Bradford A.</given-names>
</name>
<xref rid="A1" ref-type="aff">¶</xref>
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<contrib contrib-type="author"><name><surname>Atakilit</surname>
<given-names>Amha</given-names>
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<xref rid="A1" ref-type="aff">¶</xref>
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<contrib contrib-type="author"><name><surname>Sheppard</surname>
<given-names>Dean</given-names>
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<xref rid="A1" ref-type="aff">¶</xref>
<xref rid="FN1" ref-type="author-notes">§</xref>
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<aff id="A1"><label>¶</label>
From the Lung Biology Center, University of California San Francisco, Box 2922, San Francisco, CA, 94143-2922</aff>
<aff id="A2"><label>‡</label>
Thoracic Disease Research Unit, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905</aff>
</contrib-group>
<author-notes><corresp id="FN1">§ To whom correspondence should be addressed: Lung Biology Center, University of California, San Francisco, Box 2922, San Francisco, CA 94143-2922 Ph: 415-514-4270 Fax: 415-514-4278 Email:<email>deans@itsa.ucsf.edu</email>
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<pub-date pub-type="nihms-submitted"><day>12</day>
<month>10</month>
<year>2005</year>
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<pub-date pub-type="ppub"><day>11</day>
<month>2</month>
<year>2005</year>
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<pub-date pub-type="pmc-release"><day>15</day>
<month>2</month>
<year>2006</year>
</pub-date>
<volume>280</volume>
<issue>6</issue>
<fpage>4544</fpage>
<lpage>4552</lpage>
<abstract><title>Summary</title>
<p id="P2">Mice homozygous for a null mutation of the integrin α9 subunit die 6–12 days after birth from bilateral chylothoraces suggesting an underlying defect in lymphatic development. However, until now the mechanisms by which the integrin α9β1 modulates lymphangiogenesis have not been described. In this study we show that adhesion to and migration on the lymphangiogenic vascular endothelial growth factors (VEGF)-C and D are α9β1 dependent. Mouse embryonic fibroblasts and human colon carcinoma cells (SW-480) transfected to express α9β1 adhered and/or migrated on both growth factors in a concentration-dependent fashion, and both adhesion and migration were abrogated by anti-α9β1 function blocking antibody. In SW-480 cells, which lack cognate receptors for VEGFC and D, both growth factors induced α9β1-depedent Erk and paxillin phosphorylation. Human microvascular endothelial cells, which express both α9β1 and VEGF-R3, also adhered to and migrated on both growth factors, and both responses, were blocked by anti-α9β1 antibody. Furthermore, in a solid phase binding assay recombinant VEGF-C and D bound to purified α9β1 integrin in a dose- and cation-dependent fashion showing that VEGF-C and VEGF-D are ligands for the integrin α9β1. The interaction between α9β1 and VEGF-C and/or D may begin to explain the abnormal lymphatic phenotype of the α9 knockout mice.</p>
</abstract>
<contract-num rid="HL1">R01 HL064353-05</contract-num>
<contract-num rid="HL1">R01 HL064353-04</contract-num>
<contract-sponsor id="HL1">National Heart, Lung, and Blood Institute : NHLBI</contract-sponsor>
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