VEGF-C is required for intestinal lymphatic vessel maintenance and lipid absorption
Identifieur interne : 000331 ( Pmc/Curation ); précédent : 000330; suivant : 000332VEGF-C is required for intestinal lymphatic vessel maintenance and lipid absorption
Auteurs : Harri Nurmi ; Pipsa Saharinen ; Georgia Zarkada ; Wei Zheng ; Marius R. Robciuc ; Kari AlitaloSource :
- EMBO Molecular Medicine [ 1757-4676 ] ; 2015.
Abstract
Vascular endothelial growth factor C (VEGF-C) binding to its tyrosine kinase receptor VEGFR-3 drives lymphatic vessel growth during development and in pathological processes. Although the VEGF-C/VEGFR-3 pathway provides a target for treatment of cancer and lymphedema, the physiological functions of VEGF-C in adult vasculature are unknown. We show here that VEGF-C is necessary for perinatal lymphangiogenesis, but required for adult lymphatic vessel maintenance only in the intestine. Following
Url:
DOI: 10.15252/emmm.201505731
PubMed: 26459520
PubMed Central: 4644375
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<front><div type="abstract" xml:lang="en"><p>Vascular endothelial growth factor C (VEGF-C) binding to its tyrosine kinase receptor VEGFR-3 drives lymphatic vessel growth during development and in pathological processes. Although the VEGF-C/VEGFR-3 pathway provides a target for treatment of cancer and lymphedema, the physiological functions of VEGF-C in adult vasculature are unknown. We show here that VEGF-C is necessary for perinatal lymphangiogenesis, but required for adult lymphatic vessel maintenance only in the intestine. Following <italic>Vegfc</italic>
gene deletion in adult mice, the intestinal lymphatic vessels, including the lacteal vessels, underwent gradual atrophy, which was aggravated when also <italic>Vegfd</italic>
was deleted. VEGF-C was expressed by a subset of smooth muscle cells adjacent to the lacteals in the villus and in the intestinal wall. The <italic>Vegfc-</italic>
deleted mice showed defective lipid absorption and increased fecal excretion of dietary cholesterol and fatty acids. When fed a high-fat diet, the <italic>Vegfc</italic>
-deficient mice were resistant to obesity and had improved glucose metabolism. Our findings indicate that the lymphangiogenic growth factors provide trophic and dynamic regulation of the intestinal lymphatic vasculature, which could be especially important in the dietary regulation of adiposity and cholesterol metabolism.</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">EMBO Mol Med</journal-id>
<journal-id journal-id-type="iso-abbrev">EMBO Mol Med</journal-id>
<journal-id journal-id-type="publisher-id">emmm</journal-id>
<journal-title-group><journal-title>EMBO Molecular Medicine</journal-title>
</journal-title-group>
<issn pub-type="ppub">1757-4676</issn>
<issn pub-type="epub">1757-4684</issn>
<publisher><publisher-name>John Wiley & Sons, Ltd</publisher-name>
<publisher-loc>Chichester, UK</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">26459520</article-id>
<article-id pub-id-type="pmc">4644375</article-id>
<article-id pub-id-type="doi">10.15252/emmm.201505731</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Reports</subject>
</subj-group>
</article-categories>
<title-group><article-title>VEGF-C is required for intestinal lymphatic vessel maintenance and lipid absorption</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Nurmi</surname>
<given-names>Harri</given-names>
</name>
<xref ref-type="aff" rid="au1"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Saharinen</surname>
<given-names>Pipsa</given-names>
</name>
<xref ref-type="aff" rid="au1"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zarkada</surname>
<given-names>Georgia</given-names>
</name>
<xref ref-type="aff" rid="au1"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zheng</surname>
<given-names>Wei</given-names>
</name>
<xref ref-type="aff" rid="au1"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Robciuc</surname>
<given-names>Marius R</given-names>
</name>
<xref ref-type="aff" rid="au1"></xref>
<xref ref-type="author-notes" rid="fn1">†</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Alitalo</surname>
<given-names>Kari</given-names>
</name>
<xref ref-type="aff" rid="au1"></xref>
<xref ref-type="corresp" rid="cor1">*</xref>
<xref ref-type="author-notes" rid="fn1">†</xref>
</contrib>
<aff id="au1"><institution>Wihuri Research Institute and Translational Cancer Biology Program, Biomedicum Helsinki, University of Helsinki</institution>
<addr-line>Helsinki, Finland</addr-line>
</aff>
</contrib-group>
<author-notes><corresp id="cor1">* Corresponding author. Tel: +358 2 941 25511, E-mail: <email>kari.alitalo@helsinki.fi</email>
</corresp>
<fn><p><bold>Subject Categories</bold>
Development & Differentiation; Vascular Biology & Angiogenesis</p>
</fn>
<fn id="fn1"><label>†</label>
<p>These authors contributed equally to this work</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><month>11</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="epub"><day>12</day>
<month>10</month>
<year>2015</year>
</pub-date>
<volume>7</volume>
<issue>11</issue>
<fpage>1418</fpage>
<lpage>1425</lpage>
<history><date date-type="received"><day>07</day>
<month>8</month>
<year>2015</year>
</date>
<date date-type="rev-recd"><day>22</day>
<month>9</month>
<year>2015</year>
</date>
<date date-type="accepted"><day>25</day>
<month>9</month>
<year>2015</year>
</date>
</history>
<permissions><copyright-statement>© 2015 The Authors. Published under the terms of the CC BY 4.0 license</copyright-statement>
<copyright-year>2015</copyright-year>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.</license-p>
</license>
</permissions>
<abstract><p>Vascular endothelial growth factor C (VEGF-C) binding to its tyrosine kinase receptor VEGFR-3 drives lymphatic vessel growth during development and in pathological processes. Although the VEGF-C/VEGFR-3 pathway provides a target for treatment of cancer and lymphedema, the physiological functions of VEGF-C in adult vasculature are unknown. We show here that VEGF-C is necessary for perinatal lymphangiogenesis, but required for adult lymphatic vessel maintenance only in the intestine. Following <italic>Vegfc</italic>
gene deletion in adult mice, the intestinal lymphatic vessels, including the lacteal vessels, underwent gradual atrophy, which was aggravated when also <italic>Vegfd</italic>
was deleted. VEGF-C was expressed by a subset of smooth muscle cells adjacent to the lacteals in the villus and in the intestinal wall. The <italic>Vegfc-</italic>
deleted mice showed defective lipid absorption and increased fecal excretion of dietary cholesterol and fatty acids. When fed a high-fat diet, the <italic>Vegfc</italic>
-deficient mice were resistant to obesity and had improved glucose metabolism. Our findings indicate that the lymphangiogenic growth factors provide trophic and dynamic regulation of the intestinal lymphatic vasculature, which could be especially important in the dietary regulation of adiposity and cholesterol metabolism.</p>
</abstract>
<kwd-group><kwd>cholesterol</kwd>
<kwd>lipid absorption</kwd>
<kwd>lymphatic vasculature</kwd>
<kwd>obesity</kwd>
<kwd>VEGF-C</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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