Vascular Endothelial Growth Factor Receptor-2 Promotes the Development of the Lymphatic Vasculature
Identifieur interne : 001E64 ( Pmc/Checkpoint ); précédent : 001E63; suivant : 001E65Vascular Endothelial Growth Factor Receptor-2 Promotes the Development of the Lymphatic Vasculature
Auteurs : Michael T. Dellinger [États-Unis] ; Stryder M. Meadows [États-Unis] ; Katherine Wynne [États-Unis] ; Ondine Cleaver [États-Unis] ; Rolf A. Brekken [États-Unis]Source :
- PLoS ONE [ 1932-6203 ] ; 2013.
Abstract
Vascular endothelial growth factor receptor 2 (VEGFR2) is highly expressed by lymphatic endothelial cells and has been shown to stimulate lymphangiogenesis in adult mice. However, the role VEGFR2 serves in the development of the lymphatic vascular system has not been defined. Here we use the
Url:
DOI: 10.1371/journal.pone.0074686
PubMed: 24023956
PubMed Central: 3759473
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Vascular endothelial growth factor receptor 2 (VEGFR2) is highly expressed by lymphatic endothelial cells and has been shown to stimulate lymphangiogenesis in adult mice. However, the role VEGFR2 serves in the development of the lymphatic vascular system has not been defined. Here we use the <italic>Cre-lox</italic>
system to show that the proper development of the lymphatic vasculature requires VEGFR2 expression by lymphatic endothelium. We show that <italic>Lyve-1<sup>wt/Cre</sup>
;Vegfr2<sup>flox/flox</sup>
</italic>
mice possess significantly fewer dermal lymphatic vessels than <italic>Vegfr2<sup>flox/flox</sup>
</italic>
mice. Although <italic>Lyve-1<sup>wt/Cre</sup>
;Vegfr2<sup>flox/flox</sup>
</italic>
mice exhibit lymphatic hypoplasia, the lymphatic network is functional and contains all of the key features of a normal lymphatic network (initial lymphatic vessels and valved collecting vessels surrounded by smooth muscle cells (SMCs)). We also show that <italic>Lyve-1<sup>Cre</sup>
</italic>
mice display robust <italic>Cre</italic>
activity in macrophages and in blood vessels in the yolk sac, liver and lung. This activity dramatically impairs the development of blood vessels in these tissues in <italic>Lyve-1<sup>wt/Cre</sup>
;Vegfr2<sup>flox/flox</sup>
</italic>
embryos, most of which die after embryonic day14.5. Lastly, we show that inactivation of <italic>Vegfr2</italic>
in the myeloid lineage does not affect the development of the lymphatic vasculature. Therefore, the abnormal lymphatic phenotype of <italic>Lyve-1<sup>wt/Cre</sup>
;Vegfr2<sup>flox/flox</sup>
</italic>
mice is due to the deletion of <italic>Vegfr2</italic>
in the lymphatic vasculature not macrophages. Together, this work demonstrates that VEGFR2 directly promotes the expansion of the lymphatic network and further defines the molecular mechanisms controlling the development of the lymphatic vascular system.</p>
</div>
</front>
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</TEI>
<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">24023956</article-id>
<article-id pub-id-type="pmc">3759473</article-id>
<article-id pub-id-type="publisher-id">PONE-D-13-13484</article-id>
<article-id pub-id-type="doi">10.1371/journal.pone.0074686</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>Anatomy and Physiology</subject>
<subj-group><subject>Immune Physiology</subject>
<subj-group><subject>Lymphatic System</subject>
</subj-group>
</subj-group>
</subj-group>
<subj-group><subject>Developmental Biology</subject>
<subj-group><subject>Molecular Development</subject>
<subj-group><subject>Signaling</subject>
</subj-group>
</subj-group>
<subj-group><subject>Pattern Formation</subject>
</subj-group>
</subj-group>
<subj-group><subject>Genetics</subject>
<subj-group><subject>Animal Genetics</subject>
</subj-group>
</subj-group>
<subj-group><subject>Immunology</subject>
<subj-group><subject>Immunologic Techniques</subject>
<subj-group><subject>Immunohistochemical Analysis</subject>
</subj-group>
</subj-group>
</subj-group>
<subj-group><subject>Model Organisms</subject>
<subj-group><subject>Animal Models</subject>
<subj-group><subject>Mouse</subject>
</subj-group>
</subj-group>
</subj-group>
</subj-group>
<subj-group subj-group-type="Discipline-v2"><subject>Mathematics</subject>
<subj-group><subject>Statistics</subject>
<subj-group><subject>Biostatistics</subject>
</subj-group>
</subj-group>
</subj-group>
<subj-group subj-group-type="Discipline-v2"><subject>Medicine</subject>
<subj-group><subject>Anatomy and Physiology</subject>
<subj-group><subject>Immune Physiology</subject>
<subj-group><subject>Lymphatic System</subject>
</subj-group>
</subj-group>
</subj-group>
<subj-group><subject>Cardiovascular</subject>
<subj-group><subject>Vascular Biology</subject>
</subj-group>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Vascular Endothelial Growth Factor Receptor-2 Promotes the Development of the Lymphatic Vasculature</article-title>
<alt-title alt-title-type="running-head">VEGFR2 Stimulates Developmental Lymphangiogenesis</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Dellinger</surname>
<given-names>Michael T.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="corresp" rid="cor1"><sup>*</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Meadows</surname>
<given-names>Stryder M.</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Wynne</surname>
<given-names>Katherine</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cleaver</surname>
<given-names>Ondine</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Brekken</surname>
<given-names>Rolf A.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
</contrib-group>
<aff id="aff1"><label>1</label>
<addr-line>Division of Surgical Oncology, Department of Surgery, Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America</addr-line>
</aff>
<aff id="aff2"><label>2</label>
<addr-line>Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America</addr-line>
</aff>
<aff id="aff3"><label>3</label>
<addr-line>Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America</addr-line>
</aff>
<contrib-group><contrib contrib-type="editor"><name><surname>Kume</surname>
<given-names>Tsutomu</given-names>
</name>
<role>Editor</role>
<xref ref-type="aff" rid="edit1"></xref>
</contrib>
</contrib-group>
<aff id="edit1"><addr-line>Feinberg Cardiovascular Research Institute, Northwestern University, United States of America</addr-line>
</aff>
<author-notes><corresp id="cor1">* E-mail: <email>michael.dellinger@utsouthwestern.edu</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: MTD RAB. Performed the experiments: MTD KW SMM. Analyzed the data: MTD RAB. Contributed reagents/materials/analysis tools: OC. Wrote the paper: MTD RAB.</p>
</fn>
</author-notes>
<pub-date pub-type="collection"><year>2013</year>
</pub-date>
<pub-date pub-type="epub"><day>2</day>
<month>9</month>
<year>2013</year>
</pub-date>
<volume>8</volume>
<issue>9</issue>
<elocation-id>e74686</elocation-id>
<history><date date-type="received"><day>1</day>
<month>4</month>
<year>2013</year>
</date>
<date date-type="accepted"><day>8</day>
<month>8</month>
<year>2013</year>
</date>
</history>
<permissions><copyright-year>2013</copyright-year>
<copyright-holder>Dellinger 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>Vascular endothelial growth factor receptor 2 (VEGFR2) is highly expressed by lymphatic endothelial cells and has been shown to stimulate lymphangiogenesis in adult mice. However, the role VEGFR2 serves in the development of the lymphatic vascular system has not been defined. Here we use the <italic>Cre-lox</italic>
system to show that the proper development of the lymphatic vasculature requires VEGFR2 expression by lymphatic endothelium. We show that <italic>Lyve-1<sup>wt/Cre</sup>
;Vegfr2<sup>flox/flox</sup>
</italic>
mice possess significantly fewer dermal lymphatic vessels than <italic>Vegfr2<sup>flox/flox</sup>
</italic>
mice. Although <italic>Lyve-1<sup>wt/Cre</sup>
;Vegfr2<sup>flox/flox</sup>
</italic>
mice exhibit lymphatic hypoplasia, the lymphatic network is functional and contains all of the key features of a normal lymphatic network (initial lymphatic vessels and valved collecting vessels surrounded by smooth muscle cells (SMCs)). We also show that <italic>Lyve-1<sup>Cre</sup>
</italic>
mice display robust <italic>Cre</italic>
activity in macrophages and in blood vessels in the yolk sac, liver and lung. This activity dramatically impairs the development of blood vessels in these tissues in <italic>Lyve-1<sup>wt/Cre</sup>
;Vegfr2<sup>flox/flox</sup>
</italic>
embryos, most of which die after embryonic day14.5. Lastly, we show that inactivation of <italic>Vegfr2</italic>
in the myeloid lineage does not affect the development of the lymphatic vasculature. Therefore, the abnormal lymphatic phenotype of <italic>Lyve-1<sup>wt/Cre</sup>
;Vegfr2<sup>flox/flox</sup>
</italic>
mice is due to the deletion of <italic>Vegfr2</italic>
in the lymphatic vasculature not macrophages. Together, this work demonstrates that VEGFR2 directly promotes the expansion of the lymphatic network and further defines the molecular mechanisms controlling the development of the lymphatic vascular system.</p>
</abstract>
<funding-group><funding-statement>This work was supported in part by the National Institutes of Health (R01CA118240; RAB), Effie Marie Cain Scholarship (RAB), and by a Department of Defense Postdoctoral Fellowship for Breast Cancer Research (MTD). MTD was also supported by a National Institutes of Health Training Grant (T32-HL098040). 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>
<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="Cleaver, Ondine" sort="Cleaver, Ondine" uniqKey="Cleaver O" first="Ondine" last="Cleaver">Ondine Cleaver</name>
<name sortKey="Meadows, Stryder M" sort="Meadows, Stryder M" uniqKey="Meadows S" first="Stryder M." last="Meadows">Stryder M. Meadows</name>
<name sortKey="Wynne, Katherine" sort="Wynne, Katherine" uniqKey="Wynne K" first="Katherine" last="Wynne">Katherine Wynne</name>
</country>
</tree>
</affiliations>
</record>
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