Cell-Cell Interactions Influence Vascular Reprogramming by Prox1 during Embryonic Development
Identifieur interne : 004465 ( Pmc/Curation ); précédent : 004464; suivant : 004466Cell-Cell Interactions Influence Vascular Reprogramming by Prox1 during Embryonic Development
Auteurs : Harold Kim [Canada] ; Maribelle Cruz [Canada] ; Annie Bourdeau [Canada] ; Daniel J. Dumont [Canada]Source :
- PLoS ONE [ 1932-6203 ] ; 2013.
Abstract
Lymphangiogenesis is a highly regulated process that involves the reprogramming of venous endothelial cells into early lymphatic endothelial cells. This reprogramming not only displays a polarized expression pattern from the cardinal vein, but also demonstrates vascular specificity; early lymphatics only develop from the cardinal vein and not the related dorsal aorta. In our transgenic model of lymphangiogenesis, we demonstrate that Prox1 overexpression has the ability to reprogram venous endothelium but not early arterial endothelial cells
Url:
DOI: 10.1371/journal.pone.0052197
PubMed: 23341894
PubMed Central: 3544876
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PMC:3544876Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Cell-Cell Interactions Influence Vascular Reprogramming by Prox1 during Embryonic Development</title>
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<front><div type="abstract" xml:lang="en"><p>Lymphangiogenesis is a highly regulated process that involves the reprogramming of venous endothelial cells into early lymphatic endothelial cells. This reprogramming not only displays a polarized expression pattern from the cardinal vein, but also demonstrates vascular specificity; early lymphatics only develop from the cardinal vein and not the related dorsal aorta. In our transgenic model of lymphangiogenesis, we demonstrate that Prox1 overexpression has the ability to reprogram venous endothelium but not early arterial endothelial cells <italic>in vivo</italic>
, in spite of the fact that Prox1 expression is forced onto both vascular beds. Our observations suggest that this specificity during embryogenesis may be due to cell-cell interactions between the developing arterial endothelial cells and smooth muscle cells. These conclusions have far reaching implications on how we understand the vascular specificity of lymphangiogenesis.</p>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">PLoS One</journal-id>
<journal-id journal-id-type="iso-abbrev">PLoS ONE</journal-id>
<journal-id journal-id-type="publisher-id">plos</journal-id>
<journal-id journal-id-type="pmc">plosone</journal-id>
<journal-title-group><journal-title>PLoS ONE</journal-title>
</journal-title-group>
<issn pub-type="epub">1932-6203</issn>
<publisher><publisher-name>Public Library of Science</publisher-name>
<publisher-loc>San Francisco, USA</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">23341894</article-id>
<article-id pub-id-type="pmc">3544876</article-id>
<article-id pub-id-type="publisher-id">PONE-D-11-18754</article-id>
<article-id pub-id-type="doi">10.1371/journal.pone.0052197</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
</subj-group>
<subj-group subj-group-type="Discipline-v2"><subject>Biology</subject>
<subj-group><subject>Developmental Biology</subject>
<subj-group><subject>Molecular Development</subject>
<subj-group><subject>Signaling</subject>
</subj-group>
</subj-group>
<subj-group><subject>Morphogenesis</subject>
<subj-group><subject>Heart Development</subject>
</subj-group>
</subj-group>
<subj-group><subject>Cell Differentiation</subject>
<subject>Cell Fate Determination</subject>
</subj-group>
</subj-group>
<subj-group><subject>Molecular Cell Biology</subject>
<subj-group><subject>Cellular Types</subject>
<subj-group><subject>Endothelial Cells</subject>
<subject>Muscle Cells</subject>
</subj-group>
</subj-group>
</subj-group>
</subj-group>
<subj-group subj-group-type="Discipline-v2"><subject>Medicine</subject>
<subj-group><subject>Cardiovascular</subject>
<subj-group><subject>Vascular Biology</subject>
</subj-group>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Cell-Cell Interactions Influence Vascular Reprogramming by Prox1 during Embryonic Development</article-title>
<alt-title alt-title-type="running-head">Specificity of Vascular Reprogramming via Prox1</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Kim</surname>
<given-names>Harold</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cruz</surname>
<given-names>Maribelle</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bourdeau</surname>
<given-names>Annie</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Dumont</surname>
<given-names>Daniel J.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="corresp" rid="cor1"><sup>*</sup>
</xref>
</contrib>
</contrib-group>
<aff id="aff1"><label>1</label>
<addr-line>Department of Medical Biophysics, Sunnybrook Research Institute, University of Toronto, Toronto, Ontario, Canada</addr-line>
</aff>
<aff id="aff2"><label>2</label>
<addr-line>Department of Immunology, Sunnybrook Research Institute, University of Toronto, Toronto, Ontario, Canada</addr-line>
</aff>
<contrib-group><contrib contrib-type="editor"><name><surname>Luttun</surname>
<given-names>Aernout</given-names>
</name>
<role>Editor</role>
<xref ref-type="aff" rid="edit1"></xref>
</contrib>
</contrib-group>
<aff id="edit1"><addr-line>Katholieke Universiteit Leuven, Belgium</addr-line>
</aff>
<author-notes><corresp id="cor1">* E-mail: <email>dan.dumont@sri.utoronto.ca</email>
</corresp>
<fn fn-type="conflict"><p><bold>Competing Interests: </bold>
The authors have declared that no competing interests exist.</p>
</fn>
<fn fn-type="con"><p>Conceived and designed the experiments: HK DJD. Performed the experiments: HK AB. Analyzed the data: HK DJD. Contributed reagents/materials/analysis tools: MC. Wrote the paper: HK.</p>
</fn>
</author-notes>
<pub-date pub-type="collection"><year>2013</year>
</pub-date>
<pub-date pub-type="epub"><day>14</day>
<month>1</month>
<year>2013</year>
</pub-date>
<volume>8</volume>
<issue>1</issue>
<elocation-id>e52197</elocation-id>
<history><date date-type="received"><day>21</day>
<month>9</month>
<year>2011</year>
</date>
<date date-type="accepted"><day>16</day>
<month>11</month>
<year>2012</year>
</date>
</history>
<permissions><copyright-year>2013</copyright-year>
<copyright-holder>Kim et al</copyright-holder>
<license><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</license-p>
</license>
</permissions>
<abstract><p>Lymphangiogenesis is a highly regulated process that involves the reprogramming of venous endothelial cells into early lymphatic endothelial cells. This reprogramming not only displays a polarized expression pattern from the cardinal vein, but also demonstrates vascular specificity; early lymphatics only develop from the cardinal vein and not the related dorsal aorta. In our transgenic model of lymphangiogenesis, we demonstrate that Prox1 overexpression has the ability to reprogram venous endothelium but not early arterial endothelial cells <italic>in vivo</italic>
, in spite of the fact that Prox1 expression is forced onto both vascular beds. Our observations suggest that this specificity during embryogenesis may be due to cell-cell interactions between the developing arterial endothelial cells and smooth muscle cells. These conclusions have far reaching implications on how we understand the vascular specificity of lymphangiogenesis.</p>
</abstract>
<funding-group><funding-statement>Funding for this study was provided by the Heart and Stroke Foundation of Canada (T-7097). HK was awarded a Postdoctoral Fellowship from the Susan G. Komen Foundation USA (PDF0600259). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.</funding-statement>
</funding-group>
<counts><page-count count="9"></page-count>
</counts>
</article-meta>
</front>
</pmc>
</record>
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