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Essential Role of Apelin Signaling during Lymphatic Development in Zebrafish

Identifieur interne : 003A30 ( Pmc/Corpus ); précédent : 003A29; suivant : 003A31

Essential Role of Apelin Signaling during Lymphatic Development in Zebrafish

Auteurs : Jun-Dae Kim ; Yujung Kang ; Jongmin Kim ; Irinna Papangeli ; Hyeseon Kang ; Jingxia Wu ; Hyekyung Park ; Emily Nadelmann ; Stanley G. Rockson ; Hyung J. Chun ; Suk-Won Jin

Source :

Arteriosclerosis, thrombosis, and vascular biology [ 1079-5642 ] ; 2013.

RBID : PMC:3977740

Abstract

Objective

Apelin and its cognate receptor Aplnr/Apj are essential for diverse biological processes. However, the function of Apelin signaling in lymphatic development remains to be identified, despite the preferential expression of Apelin and Aplnr within developing blood (BECs) and lymphatic endothelial cells (LECs) in vertebrates. In this report, we aim to delineate the functions of Apelin signaling during lymphatic development.

Approaches and Results

We investigated the functions of Apelin signaling during lymphatic development using zebrafish embryos, and found that attenuation of Apelin signaling substantially decreased the formation of the parachordal vessel (PaCV) and the number of LECs within the developing thoracic duct, indicating an essential role of Apelin signaling during the early phase of lymphatic development. Mechanistically, we found that abrogation of Apelin signaling selectively attenuates lymphatic endothelial AKT1/2 phosphorylation without affecting the phosphorylation status of ERK1/2. Moreover, lymphatic abnormalities caused by the reduction of Apelin signaling were significantly exacerbated by the concomitant partial inhibition of AKT signaling. Apelin and Vascular Endothelial Growth Factor-C (VEGF-C) signaling provide a non-redundant activation of AKT during lymphatic development, as over-expression of VEGF-C or apelin was unable to rescue the lymphatic defects caused by the lack of Apelin or VEGF-C, respectively.

Conclusions

Taken together, our data present compelling evidence suggesting that Apelin signaling regulates lymphatic development by promoting AKT activity in a VEGF-C/VEGFR3 independent manner during zebrafish embryogenesis.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3977740

DOI: 10.1161/ATVBAHA.113.302785
PubMed: 24311379
PubMed Central: 3977740

Links to Exploration step

PMC:3977740

Le document en format XML

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<author><name sortKey="Kim, Jun Dae" sort="Kim, Jun Dae" uniqKey="Kim J" first="Jun-Dae" last="Kim">Jun-Dae Kim</name>
<affiliation><nlm:aff id="A1">Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Kang, Yujung" sort="Kang, Yujung" uniqKey="Kang Y" first="Yujung" last="Kang">Yujung Kang</name>
<affiliation><nlm:aff id="A1">Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA</nlm:aff>
</affiliation>
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<author><name sortKey="Kim, Jongmin" sort="Kim, Jongmin" uniqKey="Kim J" first="Jongmin" last="Kim">Jongmin Kim</name>
<affiliation><nlm:aff id="A2">Department of Life Systems, Sookmyung Women’s University, Seoul 140-742, Korea</nlm:aff>
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<author><name sortKey="Papangeli, Irinna" sort="Papangeli, Irinna" uniqKey="Papangeli I" first="Irinna" last="Papangeli">Irinna Papangeli</name>
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<author><name sortKey="Kang, Hyeseon" sort="Kang, Hyeseon" uniqKey="Kang H" first="Hyeseon" last="Kang">Hyeseon Kang</name>
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<author><name sortKey="Wu, Jingxia" sort="Wu, Jingxia" uniqKey="Wu J" first="Jingxia" last="Wu">Jingxia Wu</name>
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<author><name sortKey="Chun, Hyung J" sort="Chun, Hyung J" uniqKey="Chun H" first="Hyung J." last="Chun">Hyung J. Chun</name>
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<author><name sortKey="Jin, Suk Won" sort="Jin, Suk Won" uniqKey="Jin S" first="Suk-Won" last="Jin">Suk-Won Jin</name>
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<author><name sortKey="Kim, Jun Dae" sort="Kim, Jun Dae" uniqKey="Kim J" first="Jun-Dae" last="Kim">Jun-Dae Kim</name>
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<author><name sortKey="Kang, Yujung" sort="Kang, Yujung" uniqKey="Kang Y" first="Yujung" last="Kang">Yujung Kang</name>
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</affiliation>
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<author><name sortKey="Kim, Jongmin" sort="Kim, Jongmin" uniqKey="Kim J" first="Jongmin" last="Kim">Jongmin Kim</name>
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<author><name sortKey="Papangeli, Irinna" sort="Papangeli, Irinna" uniqKey="Papangeli I" first="Irinna" last="Papangeli">Irinna Papangeli</name>
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</affiliation>
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<author><name sortKey="Kang, Hyeseon" sort="Kang, Hyeseon" uniqKey="Kang H" first="Hyeseon" last="Kang">Hyeseon Kang</name>
<affiliation><nlm:aff id="A1">Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Wu, Jingxia" sort="Wu, Jingxia" uniqKey="Wu J" first="Jingxia" last="Wu">Jingxia Wu</name>
<affiliation><nlm:aff id="A1">Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA</nlm:aff>
</affiliation>
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<author><name sortKey="Park, Hyekyung" sort="Park, Hyekyung" uniqKey="Park H" first="Hyekyung" last="Park">Hyekyung Park</name>
<affiliation><nlm:aff id="A1">Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Nadelmann, Emily" sort="Nadelmann, Emily" uniqKey="Nadelmann E" first="Emily" last="Nadelmann">Emily Nadelmann</name>
<affiliation><nlm:aff id="A1">Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Rockson, Stanley G" sort="Rockson, Stanley G" uniqKey="Rockson S" first="Stanley G" last="Rockson">Stanley G. Rockson</name>
</author>
<author><name sortKey="Chun, Hyung J" sort="Chun, Hyung J" uniqKey="Chun H" first="Hyung J." last="Chun">Hyung J. Chun</name>
<affiliation><nlm:aff id="A1">Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA</nlm:aff>
</affiliation>
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<author><name sortKey="Jin, Suk Won" sort="Jin, Suk Won" uniqKey="Jin S" first="Suk-Won" last="Jin">Suk-Won Jin</name>
<affiliation><nlm:aff id="A1">Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA</nlm:aff>
</affiliation>
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<series><title level="j">Arteriosclerosis, thrombosis, and vascular biology</title>
<idno type="ISSN">1079-5642</idno>
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Objective</title>
<p id="P1">Apelin and its cognate receptor Aplnr/Apj are essential for diverse biological processes. However, the function of Apelin signaling in lymphatic development remains to be identified, despite the preferential expression of Apelin and Aplnr within developing blood (BECs) and lymphatic endothelial cells (LECs) in vertebrates. In this report, we aim to delineate the functions of Apelin signaling during lymphatic development.</p>
</sec>
<sec id="S2"><title>Approaches and Results</title>
<p id="P2">We investigated the functions of Apelin signaling during lymphatic development using zebrafish embryos, and found that attenuation of Apelin signaling substantially decreased the formation of the parachordal vessel (PaCV) and the number of LECs within the developing thoracic duct, indicating an essential role of Apelin signaling during the early phase of lymphatic development. Mechanistically, we found that abrogation of Apelin signaling selectively attenuates lymphatic endothelial AKT1/2 phosphorylation without affecting the phosphorylation status of ERK1/2. Moreover, lymphatic abnormalities caused by the reduction of Apelin signaling were significantly exacerbated by the concomitant partial inhibition of AKT signaling. Apelin and Vascular Endothelial Growth Factor-C (VEGF-C) signaling provide a non-redundant activation of AKT during lymphatic development, as over-expression of VEGF-C or apelin was unable to rescue the lymphatic defects caused by the lack of Apelin or VEGF-C, respectively.</p>
</sec>
<sec id="S3"><title>Conclusions</title>
<p id="P3">Taken together, our data present compelling evidence suggesting that Apelin signaling regulates lymphatic development by promoting AKT activity in a VEGF-C/VEGFR3 independent manner during zebrafish embryogenesis.</p>
</sec>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
  <pmc-dir>properties manuscript</pmc-dir>
  <front><journal-meta><journal-id journal-id-type="nlm-journal-id">9505803</journal-id>
<journal-id journal-id-type="pubmed-jr-id">8623</journal-id>
<journal-id journal-id-type="nlm-ta">Arterioscler Thromb Vasc Biol</journal-id>
<journal-id journal-id-type="iso-abbrev">Arterioscler. Thromb. Vasc. Biol.</journal-id>
<journal-title-group><journal-title>Arteriosclerosis, thrombosis, and vascular biology</journal-title>
</journal-title-group>
<issn pub-type="ppub">1079-5642</issn>
<issn pub-type="epub">1524-4636</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">24311379</article-id>
<article-id pub-id-type="pmc">3977740</article-id>
<article-id pub-id-type="doi">10.1161/ATVBAHA.113.302785</article-id>
<article-id pub-id-type="manuscript">NIHMS544266</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Essential Role of Apelin Signaling during Lymphatic Development in Zebrafish</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Kim</surname>
<given-names>Jun-Dae</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kang</surname>
<given-names>Yujung</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kim</surname>
<given-names>Jongmin</given-names>
</name>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Papangeli</surname>
<given-names>Irinna</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kang</surname>
<given-names>Hyeseon</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Wu</surname>
<given-names>Jingxia</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Park</surname>
<given-names>Hyekyung</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Nadelmann</surname>
<given-names>Emily</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Rockson</surname>
<given-names>Stanley G</given-names>
</name>
<xref rid="FN1" ref-type="author-notes">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chun</surname>
<given-names>Hyung J.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Jin</surname>
<given-names>Suk-Won</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref rid="FN1" ref-type="author-notes">4</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>1</label>
Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA</aff>
<aff id="A2"><label>2</label>
Department of Life Systems, Sookmyung Women’s University, Seoul 140-742, Korea</aff>
<aff id="A3"><label>3</label>
Department of Medicine, Stanford University, School of Medicine, Stanford, CA94305, USA</aff>
<author-notes><corresp id="FN1"><label>4</label>
To whom correspondence should be addressed. <email>suk-won.jin@yale.edu</email>
 or <email>hyung.chun@yale.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>9</day>
<month>1</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="epub"><day>05</day>
<month>12</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="ppub"><month>2</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>01</day>
<month>2</month>
<year>2015</year>
</pub-date>
<volume>34</volume>
<issue>2</issue>
<fpage>338</fpage>
<lpage>345</lpage>
<pmc-comment>elocation-id from pubmed: 10.1161/ATVBAHA.113.302785</pmc-comment>
      <abstract><sec id="S1"><title>Objective</title>
<p id="P1">Apelin and its cognate receptor Aplnr/Apj are essential for diverse biological processes. However, the function of Apelin signaling in lymphatic development remains to be identified, despite the preferential expression of Apelin and Aplnr within developing blood (BECs) and lymphatic endothelial cells (LECs) in vertebrates. In this report, we aim to delineate the functions of Apelin signaling during lymphatic development.</p>
</sec>
<sec id="S2"><title>Approaches and Results</title>
<p id="P2">We investigated the functions of Apelin signaling during lymphatic development using zebrafish embryos, and found that attenuation of Apelin signaling substantially decreased the formation of the parachordal vessel (PaCV) and the number of LECs within the developing thoracic duct, indicating an essential role of Apelin signaling during the early phase of lymphatic development. Mechanistically, we found that abrogation of Apelin signaling selectively attenuates lymphatic endothelial AKT1/2 phosphorylation without affecting the phosphorylation status of ERK1/2. Moreover, lymphatic abnormalities caused by the reduction of Apelin signaling were significantly exacerbated by the concomitant partial inhibition of AKT signaling. Apelin and Vascular Endothelial Growth Factor-C (VEGF-C) signaling provide a non-redundant activation of AKT during lymphatic development, as over-expression of VEGF-C or apelin was unable to rescue the lymphatic defects caused by the lack of Apelin or VEGF-C, respectively.</p>
</sec>
<sec id="S3"><title>Conclusions</title>
<p id="P3">Taken together, our data present compelling evidence suggesting that Apelin signaling regulates lymphatic development by promoting AKT activity in a VEGF-C/VEGFR3 independent manner during zebrafish embryogenesis.</p>
</sec>
</abstract>
<kwd-group><kwd>Apelin signaling</kwd>
<kwd>Lymphatic development</kwd>
<kwd>AKT</kwd>
<kwd>Zebrafish</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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Essential Role of Apelin Signaling during Lymphatic Development in Zebrafish

Essential Role of Apelin Signaling during Lymphatic Development in Zebrafish

Source :

Abstract

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki