An essential role for Prox1 in the induction of the lymphatic endothelial cell phenotype
Identifieur interne : 001E74 ( Istex/Corpus ); précédent : 001E73; suivant : 001E75An essential role for Prox1 in the induction of the lymphatic endothelial cell phenotype
Auteurs : Jeffrey T. Wigle ; Natasha Harvey ; Michael Detmar ; Irina Lagutina ; Gerard Grosveld ; Michael D. Gunn ; David G. Jackson ; Guillermo OliverSource :
- The EMBO Journal [ 0261-4189 ] ; 2002-04-01.
Abstract
The process of angiogenesis has been well documented, but little is known about the biology of lymphatic endothelial cells and the molecular mechanisms controlling lymphangiogenesis. The homeobox gene Prox1 is expressed in a subpopulation of endothelial cells that, after budding from veins, gives rise to the mammalian lymphatic system. In Prox1−/− embryos, this budding becomes arrested at around embryonic day (E)11.5, resulting in embryos without lymphatic vasculature. Unlike the endothelial cells that bud off in E11.5 wild‐type embryos, those of Prox1‐null embryos did not co‐express any lymphatic markers such as VEGFR‐3, LYVE‐1 or SLC. Instead, the mutant cells appeared to have a blood vascular phenotype, as determined by their expression of laminin and CD34. These results suggest that Prox1 activity is required for both maintenance of the budding of the venous endothelial cells and differentiation toward the lymphatic phenotype. On the basis of our findings, we propose that a blood vascular phenotype is the default fate of budding embryonic venous endothelial cells; upon expression of Prox1, these budding cells adopt a lymphatic vasculature phenotype.
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DOI: 10.1093/emboj/21.7.1505
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ISTEX:430BFF725DBFA4AABFD1C302051944C214642EDELe document en format XML
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Wigle</name><affiliation><mods:affiliation>Department of Genetics, St Jude Children's Research Hospital, 38105, Memphis, TN, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Present address: Division of Stroke and Vascular Disease and Department of Biochemistry and Medical Genetics, St Boniface General Hospital Research Centre, Winnipeg, Canada</mods:affiliation></affiliation></author><author><name sortKey="Harvey, Natasha" sort="Harvey, Natasha" uniqKey="Harvey N" first="Natasha" last="Harvey">Natasha Harvey</name><affiliation><mods:affiliation>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</mods:affiliation></affiliation></author><author><name sortKey="Detmar, Michael" sort="Detmar, Michael" uniqKey="Detmar M" first="Michael" last="Detmar">Michael Detmar</name><affiliation><mods:affiliation>Cutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, MA, 02114, Boston, USA</mods:affiliation></affiliation></author><author><name sortKey="Lagutina, Irina" sort="Lagutina, Irina" uniqKey="Lagutina I" first="Irina" last="Lagutina">Irina Lagutina</name><affiliation><mods:affiliation>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</mods:affiliation></affiliation></author><author><name sortKey="Grosveld, Gerard" sort="Grosveld, Gerard" uniqKey="Grosveld G" first="Gerard" last="Grosveld">Gerard Grosveld</name><affiliation><mods:affiliation>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</mods:affiliation></affiliation></author><author><name sortKey="Gunn, Michael D" sort="Gunn, Michael D" uniqKey="Gunn M" first="Michael D." last="Gunn">Michael D. 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Wigle</name><affiliation><mods:affiliation>Department of Genetics, St Jude Children's Research Hospital, 38105, Memphis, TN, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Present address: Division of Stroke and Vascular Disease and Department of Biochemistry and Medical Genetics, St Boniface General Hospital Research Centre, Winnipeg, Canada</mods:affiliation></affiliation></author><author><name sortKey="Harvey, Natasha" sort="Harvey, Natasha" uniqKey="Harvey N" first="Natasha" last="Harvey">Natasha Harvey</name><affiliation><mods:affiliation>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</mods:affiliation></affiliation></author><author><name sortKey="Detmar, Michael" sort="Detmar, Michael" uniqKey="Detmar M" first="Michael" last="Detmar">Michael Detmar</name><affiliation><mods:affiliation>Cutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, MA, 02114, Boston, USA</mods:affiliation></affiliation></author><author><name sortKey="Lagutina, Irina" sort="Lagutina, Irina" uniqKey="Lagutina I" first="Irina" last="Lagutina">Irina Lagutina</name><affiliation><mods:affiliation>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</mods:affiliation></affiliation></author><author><name sortKey="Grosveld, Gerard" sort="Grosveld, Gerard" uniqKey="Grosveld G" first="Gerard" last="Grosveld">Gerard Grosveld</name><affiliation><mods:affiliation>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</mods:affiliation></affiliation></author><author><name sortKey="Gunn, Michael D" sort="Gunn, Michael D" uniqKey="Gunn M" first="Michael D." last="Gunn">Michael D. 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Jackson</name><affiliation><mods:affiliation>MRC Human Immunology Unit, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, OX3 9DS, Headington, UK</mods:affiliation></affiliation></author><author><name sortKey="Oliver, Guillermo" sort="Oliver, Guillermo" uniqKey="Oliver G" first="Guillermo" last="Oliver">Guillermo Oliver</name><affiliation><mods:affiliation>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: guillermo.oliver@stjude.org</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">The EMBO Journal</title><title level="j" type="alt">THE EMBO JOURNAL</title><idno type="ISSN">0261-4189</idno><idno type="eISSN">1460-2075</idno><imprint><biblScope unit="vol">21</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="1505">1505</biblScope><biblScope unit="page" to="1513">1513</biblScope><biblScope unit="page-count">9</biblScope><publisher>John Wiley & Sons, Ltd</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2002-04-01">2002-04-01</date></imprint><idno type="ISSN">0261-4189</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0261-4189</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">The process of angiogenesis has been well documented, but little is known about the biology of lymphatic endothelial cells and the molecular mechanisms controlling lymphangiogenesis. The homeobox gene Prox1 is expressed in a subpopulation of endothelial cells that, after budding from veins, gives rise to the mammalian lymphatic system. In Prox1−/− embryos, this budding becomes arrested at around embryonic day (E)11.5, resulting in embryos without lymphatic vasculature. Unlike the endothelial cells that bud off in E11.5 wild‐type embryos, those of Prox1‐null embryos did not co‐express any lymphatic markers such as VEGFR‐3, LYVE‐1 or SLC. Instead, the mutant cells appeared to have a blood vascular phenotype, as determined by their expression of laminin and CD34. These results suggest that Prox1 activity is required for both maintenance of the budding of the venous endothelial cells and differentiation toward the lymphatic phenotype. On the basis of our findings, we propose that a blood vascular phenotype is the default fate of budding embryonic venous endothelial cells; upon expression of Prox1, these budding cells adopt a lymphatic vasculature phenotype.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>lymphatic</json:string><json:string>prox1</json:string><json:string>endothelial cells</json:string><json:string>endothelial</json:string><json:string>embryo</json:string><json:string>vasculature</json:string><json:string>cardinal vein</json:string><json:string>lymphangiogenesis</json:string><json:string>nullizygous</json:string><json:string>lymphatic vasculature</json:string><json:string>wigle</json:string><json:string>subpopulation</json:string><json:string>high levels</json:string><json:string>laminin</json:string><json:string>phenotype</json:string><json:string>venous</json:string><json:string>lymphatic vessels</json:string><json:string>chemokine</json:string><json:string>receptor</json:string><json:string>prox1 activity</json:string><json:string>lymphatic markers</json:string><json:string>heterozygous embryos</json:string><json:string>mutant</json:string><json:string>littermates</json:string><json:string>lymphatic system</json:string><json:string>endothelium</json:string><json:string>prox1 function</json:string><json:string>arrowhead</json:string><json:string>lymphatic endothelium</json:string><json:string>blood vessels</json:string><json:string>heterozygous</json:string><json:string>prox1 expression</json:string><json:string>adjacent sections</json:string><json:string>marker</json:string><json:string>vascular system</json:string><json:string>mutant littermates</json:string><json:string>tumor lymphangiogenesis</json:string><json:string>lymphatic pathway</json:string><json:string>embryonic veins</json:string><json:string>lymphatic capillaries</json:string><json:string>nullizygous embryos</json:string><json:string>immunohistochemical analyses</json:string><json:string>endothelial cell</json:string><json:string>prox1 nullizygous embryos</json:string><json:string>lymphatic differentiation program</json:string><json:string>lymphatic bias</json:string><json:string>natl acad</json:string></teeft></keywords><author><json:item><name>Jeffrey T. Wigle</name><affiliations><json:string>Department of Genetics, St Jude Children's Research Hospital, 38105, Memphis, TN, USA</json:string><json:string>Present address: Division of Stroke and Vascular Disease and Department of Biochemistry and Medical Genetics, St Boniface General Hospital Research Centre, Winnipeg, Canada</json:string></affiliations></json:item><json:item><name>Natasha Harvey</name><affiliations><json:string>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</json:string></affiliations></json:item><json:item><name>Michael Detmar</name><affiliations><json:string>Cutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, MA, 02114, Boston, USA</json:string></affiliations></json:item><json:item><name>Irina Lagutina</name><affiliations><json:string>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</json:string></affiliations></json:item><json:item><name>Gerard Grosveld</name><affiliations><json:string>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</json:string></affiliations></json:item><json:item><name>Michael D. Gunn</name><affiliations><json:string>Division of Cardiology, Department of Medicine, Duke University Medical Center, NC, 27710, Durham, USA</json:string></affiliations></json:item><json:item><name>David G. Jackson</name><affiliations><json:string>MRC Human Immunology Unit, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, OX3 9DS, Headington, UK</json:string></affiliations></json:item><json:item><name>Guillermo Oliver</name><affiliations><json:string>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</json:string><json:string>E-mail: guillermo.oliver@stjude.org</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>lymphangiogenesis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>lymphatic endothelial cells</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>LYVE‐1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Prox1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SLC</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>VEGFR‐3</value></json:item></subject><articleId><json:string>EMBJ7594370</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>The process of angiogenesis has been well documented, but little is known about the biology of lymphatic endothelial cells and the molecular mechanisms controlling lymphangiogenesis. The homeobox gene Prox1 is expressed in a subpopulation of endothelial cells that, after budding from veins, gives rise to the mammalian lymphatic system. In Prox1−/− embryos, this budding becomes arrested at around embryonic day (E)11.5, resulting in embryos without lymphatic vasculature. Unlike the endothelial cells that bud off in E11.5 wild‐type embryos, those of Prox1‐null embryos did not co‐express any lymphatic markers such as VEGFR‐3, LYVE‐1 or SLC. Instead, the mutant cells appeared to have a blood vascular phenotype, as determined by their expression of laminin and CD34. These results suggest that Prox1 activity is required for both maintenance of the budding of the venous endothelial cells and differentiation toward the lymphatic phenotype. 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Hospital</orgName><address><settlement type="city">Memphis</settlement><postCode>38105</postCode><region>TN</region><country key="US">USA</country></address></affiliation><affiliation><orgName>Present address: Division of Stroke and Vascular Disease and Department of Biochemistry and Medical Genetics, St Boniface General Hospital Research Centre</orgName><address><region>Winnipeg</region><country key="CA">Canada</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Natasha</forename><surname>Harvey</surname></persName><affiliation><orgName>Department of Genetics, St Jude Children's Research Hospital</orgName><address><settlement type="city">Memphis</settlement><postCode>38105</postCode><region>TN</region><country key="US">USA</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Michael</forename><surname>Detmar</surname></persName><affiliation><orgName>Cutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School</orgName><address><settlement type="city">Boston</settlement><postCode>02114</postCode><region>MA</region><country key="US">USA</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Irina</forename><surname>Lagutina</surname></persName><affiliation><orgName>Department of Genetics, St Jude Children's Research Hospital</orgName><address><settlement type="city">Memphis</settlement><postCode>38105</postCode><region>TN</region><country key="US">USA</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Gerard</forename><surname>Grosveld</surname></persName><affiliation><orgName>Department of Genetics, St Jude Children's Research Hospital</orgName><address><settlement type="city">Memphis</settlement><postCode>38105</postCode><region>TN</region><country key="US">USA</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Michael D.</forename><surname>Gunn</surname></persName><affiliation><orgName>Division of Cardiology, Department of Medicine, Duke University Medical Center</orgName><address><settlement type="city">Durham</settlement><postCode>27710</postCode><region>NC</region><country key="US">USA</country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">David G.</forename><surname>Jackson</surname></persName><affiliation><orgName>MRC Human Immunology Unit, Institute of Molecular Medicine, John Radcliffe Hospital</orgName><address><settlement type="city">Headington</settlement><postCode>OX3 9DS</postCode><region>Oxford</region><country key="GB">UK</country></address></affiliation></author><author xml:id="author-0007" role="corresp"><persName><forename type="first">Guillermo</forename><surname>Oliver</surname></persName><affiliation><orgName>Department of Genetics, St Jude Children's Research Hospital</orgName><address><settlement type="city">Memphis</settlement><postCode>38105</postCode><region>TN</region><country key="US">USA</country></address></affiliation><affiliation>Corresponding author. E‐mail: guillermo.oliver@stjude.org</affiliation></author><idno type="istex">430BFF725DBFA4AABFD1C302051944C214642EDE</idno><idno type="DOI">10.1093/emboj/21.7.1505</idno><idno type="unit">EMBJ7594370</idno><idno type="toTypesetVersion">file:EMBJ.EMBJ7594370.pdf</idno></analytic><monogr><title level="j" type="main">The EMBO Journal</title><title level="j" type="alt">THE EMBO JOURNAL</title><idno type="pISSN">0261-4189</idno><idno type="eISSN">1460-2075</idno><idno type="book-DOI">10.1002/(ISSN)1460-2075</idno><idno type="book-part-DOI">10.1002/emboj.v21.7</idno><idno type="product">EMBJ</idno><imprint><biblScope unit="vol">21</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="1505">1505</biblScope><biblScope unit="page" to="1513">1513</biblScope><biblScope unit="page-count">9</biblScope><publisher>John Wiley & Sons, Ltd</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2002-04-01"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract style="main"><p>The process of angiogenesis has been well documented, but little is known about the biology of lymphatic endothelial cells and the molecular mechanisms controlling lymphangiogenesis. The homeobox gene <hi rend="italic">Prox1</hi> is expressed in a subpopulation of endothelial cells that, after budding from veins, gives rise to the mammalian lymphatic system. In <hi rend="italic">Prox1<hi rend="superscript">−/−</hi></hi> embryos, this budding becomes arrested at around embryonic day (E)11.5, resulting in embryos without lymphatic vasculature. Unlike the endothelial cells that bud off in E11.5 wild‐type embryos, those of <hi rend="italic">Prox1‐</hi>null embryos did not co‐express any lymphatic markers such as VEGFR‐3, LYVE‐1 or SLC. Instead, the mutant cells appeared to have a blood vascular phenotype, as determined by their expression of laminin and CD34. These results suggest that <hi rend="italic">Prox1</hi> activity is required for both maintenance of the budding of the venous endothelial cells and differentiation toward the lymphatic phenotype. On the basis of our findings, we propose that a blood vascular phenotype is the default fate of budding embryonic venous endothelial cells; upon expression of Prox1, these budding cells adopt a lymphatic vasculature phenotype.</p></abstract><textClass><keywords><term xml:id="embj7594370-kwd-0001">lymphangiogenesis</term><term xml:id="embj7594370-kwd-0002">lymphatic endothelial cells</term><term xml:id="embj7594370-kwd-0003">LYVE‐1</term><term xml:id="embj7594370-kwd-0004">Prox1</term><term xml:id="embj7594370-kwd-0005">SLC</term><term xml:id="embj7594370-kwd-0006">VEGFR‐3</term></keywords><classCode scheme="http://psi.embo.org/14602075/EMBO09">Chromatin, Epigenetics, Genomics & Functional Genomics</classCode><classCode scheme="http://psi.embo.org/14602075/EMBO07">Cell Death & Autophagy</classCode><classCode scheme="articleCategory">Article</classCode><classCode scheme="tocHeading1">Article</classCode></textClass><langUsage><language ident="EN"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/430BFF725DBFA4AABFD1C302051944C214642EDE/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component type="serialArticle" version="2.0" xml:lang="en" xml:id="embj7594370"><header><publicationMeta level="product"><publisherInfo><publisherName>John Wiley & Sons, Ltd</publisherName><publisherLoc>Chichester, UK</publisherLoc></publisherInfo><doi>10.1002/(ISSN)1460-2075</doi><issn type="print">0261-4189</issn><issn type="electronic">1460-2075</issn><idGroup><id type="product" value="EMBJ"></id></idGroup><titleGroup><title type="main" sort="THE EMBO JOURNAL">The EMBO Journal</title></titleGroup></publicationMeta><publicationMeta level="part" position="70"><doi>10.1002/emboj.v21.7</doi><copyright ownership="publisher">Copyright © 2013 Wiley Periodicals, Inc</copyright><numberingGroup><numbering type="journalVolume" number="21">21</numbering><numbering type="journalIssue">7</numbering></numberingGroup><coverDate startDate="2002-04-01">April 1, 2002</coverDate></publicationMeta><publicationMeta level="unit" position="10" type="article" status="forIssue"><doi>10.1093/emboj/21.7.1505</doi><idGroup><id type="unit" value="EMBJ7594370"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup>
<title type="articleCategory">Article</title><title type="tocHeading1">Article</title></titleGroup><copyright ownership="thirdParty">Copyright © 2002 European Molecular Biology Organization</copyright><eventGroup><event type="manuscriptReceived" date="2001-12-17"></event><event type="manuscriptRevised" date="2002-01-22"></event><event type="manuscriptAccepted" date="2002-01-31"></event><event type="publishedOnlineFinalForm" date="2002-04-01"></event><event type="xmlConverted" agent="SPi Global Converter_TO_WileyML3Gv2.0 version:1.0; WileyML 3G Packaging Tool v1.0" date="2013-10-12"></event><event type="firstOnline" date="2002-04-01"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-04"></event></eventGroup><numberingGroup><numbering type="pageFirst">1505</numbering><numbering type="pageLast">1513</numbering></numberingGroup><correspondenceTo>Corresponding author. E‐mail: <email>guillermo.oliver@stjude.org</email></correspondenceTo><subjectInfo><subject href="http://psi.embo.org/14602075/EMBO09">Chromatin, Epigenetics, Genomics & Functional Genomics</subject><subject href="http://psi.embo.org/14602075/EMBO07">Cell Death & Autophagy</subject></subjectInfo><linkGroup><link type="toTypesetVersion" href="file:EMBJ.EMBJ7594370.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">An essential role for <i>Prox1</i> in the induction of the lymphatic endothelial cell phenotype</title></titleGroup><creators><creator creatorRole="author" xml:id="embj7594370-cr-0001" affiliationRef="#embj7594370-aff-0001 #embj7594370-aff-0002"><personName><givenNames>Jeffrey T.</givenNames><familyName>Wigle</familyName></personName></creator><creator creatorRole="author" xml:id="embj7594370-cr-0002" affiliationRef="#embj7594370-aff-0001"><personName><givenNames>Natasha</givenNames><familyName>Harvey</familyName></personName></creator><creator creatorRole="author" xml:id="embj7594370-cr-0003" affiliationRef="#embj7594370-aff-0003"><personName><givenNames>Michael</givenNames><familyName>Detmar</familyName></personName></creator><creator creatorRole="author" xml:id="embj7594370-cr-0004" affiliationRef="#embj7594370-aff-0001"><personName><givenNames>Irina</givenNames><familyName>Lagutina</familyName></personName></creator><creator creatorRole="author" xml:id="embj7594370-cr-0005" affiliationRef="#embj7594370-aff-0001"><personName><givenNames>Gerard</givenNames><familyName>Grosveld</familyName></personName></creator><creator creatorRole="author" xml:id="embj7594370-cr-0006" affiliationRef="#embj7594370-aff-0004"><personName><givenNames>Michael D.</givenNames><familyName>Gunn</familyName></personName></creator><creator creatorRole="author" xml:id="embj7594370-cr-0007" affiliationRef="#embj7594370-aff-0005"><personName><givenNames>David G.</givenNames><familyName>Jackson</familyName></personName></creator><creator creatorRole="author" xml:id="embj7594370-cr-0008" affiliationRef="#embj7594370-aff-0001" corresponding="yes"><personName><givenNames>Guillermo</givenNames><familyName>Oliver</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="US" type="organization" xml:id="embj7594370-aff-0001"><orgName>Department of Genetics, St Jude Children's Research Hospital</orgName><address><city>Memphis</city><countryPart>TN</countryPart><postCode>38105</postCode><country>USA</country></address></affiliation><affiliation countryCode="CA" type="organization" xml:id="embj7594370-aff-0002"><orgName>Present address: Division of Stroke and Vascular Disease and Department of Biochemistry and Medical Genetics, St Boniface General Hospital Research Centre</orgName><address><countryPart>Winnipeg</countryPart><country>Canada</country></address></affiliation><affiliation countryCode="US" type="organization" xml:id="embj7594370-aff-0003"><orgName>Cutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School</orgName><address><city>Boston</city><countryPart>MA</countryPart><postCode>02114</postCode><country>USA</country></address></affiliation><affiliation countryCode="US" type="organization" xml:id="embj7594370-aff-0004"><orgName>Division of Cardiology, Department of Medicine, Duke University Medical Center</orgName><address><city>Durham</city><countryPart>NC</countryPart><postCode>27710</postCode><country>USA</country></address></affiliation><affiliation countryCode="GB" type="organization" xml:id="embj7594370-aff-0005"><orgName>MRC Human Immunology Unit, Institute of Molecular Medicine, John Radcliffe Hospital</orgName><address><city>Headington</city><countryPart>Oxford</countryPart><postCode>OX3 9DS</postCode><country>UK</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="embj7594370-kwd-0001">lymphangiogenesis</keyword><keyword xml:id="embj7594370-kwd-0002">lymphatic endothelial cells</keyword><keyword xml:id="embj7594370-kwd-0003">LYVE‐1</keyword><keyword xml:id="embj7594370-kwd-0004">Prox1</keyword><keyword xml:id="embj7594370-kwd-0005">SLC</keyword><keyword xml:id="embj7594370-kwd-0006">VEGFR‐3</keyword></keywordGroup><abstractGroup><abstract type="main"><p>The process of angiogenesis has been well documented, but little is known about the biology of lymphatic endothelial cells and the molecular mechanisms controlling lymphangiogenesis. The homeobox gene <i>Prox1</i> is expressed in a subpopulation of endothelial cells that, after budding from veins, gives rise to the mammalian lymphatic system. In <i>Prox1<sup>−/−</sup></i> embryos, this budding becomes arrested at around embryonic day (E)11.5, resulting in embryos without lymphatic vasculature. Unlike the endothelial cells that bud off in E11.5 wild‐type embryos, those of <i>Prox1‐</i>null embryos did not co‐express any lymphatic markers such as VEGFR‐3, LYVE‐1 or SLC. Instead, the mutant cells appeared to have a blood vascular phenotype, as determined by their expression of laminin and CD34. These results suggest that <i>Prox1</i> activity is required for both maintenance of the budding of the venous endothelial cells and differentiation toward the lymphatic phenotype. On the basis of our findings, we propose that a blood vascular phenotype is the default fate of budding embryonic venous endothelial cells; upon expression of Prox1, these budding cells adopt a lymphatic vasculature phenotype.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>An essential role for Prox1 in the induction of the lymphatic endothelial cell phenotype</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>An essential role for Prox1 in the induction of the lymphatic endothelial cell phenotype</title></titleInfo><name type="personal"><namePart type="given">Jeffrey T.</namePart><namePart type="family">Wigle</namePart><affiliation>Department of Genetics, St Jude Children's Research Hospital, 38105, Memphis, TN, USA</affiliation><affiliation>Present address: Division of Stroke and Vascular Disease and Department of Biochemistry and Medical Genetics, St Boniface General Hospital Research Centre, Winnipeg, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Natasha</namePart><namePart type="family">Harvey</namePart><affiliation>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Detmar</namePart><affiliation>Cutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, MA, 02114, Boston, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Irina</namePart><namePart type="family">Lagutina</namePart><affiliation>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gerard</namePart><namePart type="family">Grosveld</namePart><affiliation>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael D.</namePart><namePart type="family">Gunn</namePart><affiliation>Division of Cardiology, Department of Medicine, Duke University Medical Center, NC, 27710, Durham, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David G.</namePart><namePart type="family">Jackson</namePart><affiliation>MRC Human Immunology Unit, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, OX3 9DS, Headington, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Guillermo</namePart><namePart type="family">Oliver</namePart><affiliation>Department of Genetics, St Jude Children's Research Hospital, TN, 38105, Memphis, USA</affiliation><affiliation>E-mail: guillermo.oliver@stjude.org</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Ltd</publisher><place><placeTerm type="text">Chichester, UK</placeTerm></place><dateIssued encoding="w3cdtf">2002-04-01</dateIssued><dateCaptured encoding="w3cdtf">2001-12-17</dateCaptured><dateValid encoding="w3cdtf">2002-01-31</dateValid><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>The process of angiogenesis has been well documented, but little is known about the biology of lymphatic endothelial cells and the molecular mechanisms controlling lymphangiogenesis. The homeobox gene Prox1 is expressed in a subpopulation of endothelial cells that, after budding from veins, gives rise to the mammalian lymphatic system. In Prox1−/− embryos, this budding becomes arrested at around embryonic day (E)11.5, resulting in embryos without lymphatic vasculature. Unlike the endothelial cells that bud off in E11.5 wild‐type embryos, those of Prox1‐null embryos did not co‐express any lymphatic markers such as VEGFR‐3, LYVE‐1 or SLC. Instead, the mutant cells appeared to have a blood vascular phenotype, as determined by their expression of laminin and CD34. These results suggest that Prox1 activity is required for both maintenance of the budding of the venous endothelial cells and differentiation toward the lymphatic phenotype. On the basis of our findings, we propose that a blood vascular phenotype is the default fate of budding embryonic venous endothelial cells; upon expression of Prox1, these budding cells adopt a lymphatic vasculature phenotype.</abstract><subject><genre>keywords</genre><topic>lymphangiogenesis</topic><topic>lymphatic endothelial cells</topic><topic>LYVE‐1</topic><topic>Prox1</topic><topic>SLC</topic><topic>VEGFR‐3</topic></subject><relatedItem type="host"><titleInfo><title>The EMBO Journal</title></titleInfo><genre type="journal">journal</genre><subject><genre>index-terms</genre><topic authorityURI="http://psi.embo.org/14602075/EMBO09">Chromatin, Epigenetics, Genomics & Functional Genomics</topic><topic authorityURI="http://psi.embo.org/14602075/EMBO07">Cell Death & Autophagy</topic></subject><subject><genre>article-category</genre><topic>Article</topic></subject><identifier type="ISSN">0261-4189</identifier><identifier type="eISSN">1460-2075</identifier><identifier type="DOI">10.1002/(ISSN)1460-2075</identifier><identifier type="PublisherID">EMBJ</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>1505</start><end>1513</end><total>9</total></extent></part></relatedItem><identifier type="istex">430BFF725DBFA4AABFD1C302051944C214642EDE</identifier><identifier type="DOI">10.1093/emboj/21.7.1505</identifier><identifier type="ArticleID">EMBJ7594370</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2013 Wiley Periodicals, IncCopyright © 2002 European Molecular Biology Organization</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>John Wiley & Sons, Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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