The KSHV viral IL-6 homolog is sufficient to induce blood to lymphatic endothelial cell differentiation
Identifieur interne : 004C95 ( Ncbi/Merge ); précédent : 004C94; suivant : 004C96The KSHV viral IL-6 homolog is sufficient to induce blood to lymphatic endothelial cell differentiation
Auteurs : Valerie A. Morris [États-Unis] ; Almira S. Punjabi [États-Unis] ; Robert C. Wells [États-Unis] ; Cristina J. Wittkopp [États-Unis] ; Richard Vart [Royaume-Uni] ; Michael Lagunoff [États-Unis]Source :
- Virology [ 0042-6822 ] ; 2012.
Abstract
The predominant tumor cell of Kaposi’s Sarcoma (KS) is the spindle cell, a cell of endothelial origin that expresses markers of lymphatic endothelium. In culture, Kaposi’s Sarcoma-associated herpesvirus (KSHV) infection of blood endothelial cells drives expression of lymphatic endothelial cell specific markers, in a process that requires activation of the gp130 receptor and the JAK2/STAT3 and PI3K/AKT signaling pathways. While expression of each of the KSHV major latent genes in endothelial cells failed to increase expression of lymphatic markers, the viral homolog of human IL-6 (vIL-6) was sufficient for induction and requires the JAK2/STAT3 and PI3K/AKT pathways. Therefore, activation of gp130 and downstream signaling by vIL-6 is sufficient to drive blood to lymphatic endothelial cell differentiation. While sufficient, vIL-6 is not necessary for lymphatic reprogramming in the context of viral infection. This indicates that multiple viral genes are involved and suggests a central importance of this pathway to KSHV pathogenesis.
Url:
DOI: 10.1016/j.virol.2012.03.013
PubMed: 22521915
PubMed Central: 3509939
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Morris</name><affiliation wicri:level="4"><nlm:aff id="A1">Department of Microbiology, University of Washington, Seattle, WA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, University of Washington, Seattle, WA</wicri:regionArea><orgName type="university">Université de Washington</orgName><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Punjabi, Almira S" sort="Punjabi, Almira S" uniqKey="Punjabi A" first="Almira S." last="Punjabi">Almira S. Punjabi</name><affiliation wicri:level="4"><nlm:aff id="A1">Department of Microbiology, University of Washington, Seattle, WA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, University of Washington, Seattle, WA</wicri:regionArea><orgName type="university">Université de Washington</orgName><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Wells, Robert C" sort="Wells, Robert C" uniqKey="Wells R" first="Robert C." last="Wells">Robert C. Wells</name><affiliation wicri:level="4"><nlm:aff id="A1">Department of Microbiology, University of Washington, Seattle, WA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, University of Washington, Seattle, WA</wicri:regionArea><orgName type="university">Université de Washington</orgName><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Wittkopp, Cristina J" sort="Wittkopp, Cristina J" uniqKey="Wittkopp C" first="Cristina J." last="Wittkopp">Cristina J. 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In culture, Kaposi’s Sarcoma-associated herpesvirus (KSHV) infection of blood endothelial cells drives expression of lymphatic endothelial cell specific markers, in a process that requires activation of the gp130 receptor and the JAK2/STAT3 and PI3K/AKT signaling pathways. While expression of each of the KSHV major latent genes in endothelial cells failed to increase expression of lymphatic markers, the viral homolog of human IL-6 (vIL-6) was sufficient for induction and requires the JAK2/STAT3 and PI3K/AKT pathways. Therefore, activation of gp130 and downstream signaling by vIL-6 is sufficient to drive blood to lymphatic endothelial cell differentiation. While sufficient, vIL-6 is not necessary for lymphatic reprogramming in the context of viral infection. This indicates that multiple viral genes are involved and suggests a central importance of this pathway to KSHV pathogenesis.</p></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">0110674</journal-id><journal-id journal-id-type="pubmed-jr-id">8015</journal-id><journal-id journal-id-type="nlm-ta">Virology</journal-id><journal-id journal-id-type="iso-abbrev">Virology</journal-id><journal-title-group><journal-title>Virology</journal-title></journal-title-group><issn pub-type="ppub">0042-6822</issn><issn pub-type="epub">1096-0341</issn></journal-meta><article-meta><article-id pub-id-type="pmid">22521915</article-id><article-id pub-id-type="pmc">3509939</article-id><article-id pub-id-type="doi">10.1016/j.virol.2012.03.013</article-id><article-id pub-id-type="manuscript">NIHMS379677</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>The KSHV viral IL-6 homolog is sufficient to induce blood to lymphatic endothelial cell differentiation</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Morris</surname><given-names>Valerie A.</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Punjabi</surname><given-names>Almira S.</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Wells</surname><given-names>Robert C.</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Wittkopp</surname><given-names>Cristina J.</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Vart</surname><given-names>Richard</given-names></name><xref ref-type="aff" rid="A2">b</xref></contrib><contrib contrib-type="author"><name><surname>Lagunoff</surname><given-names>Michael</given-names></name><xref ref-type="aff" rid="A1">a</xref><xref rid="FN1" ref-type="author-notes">*</xref></contrib></contrib-group><aff id="A1"><label>a</label>Department of Microbiology, University of Washington, Seattle, WA, USA</aff><aff id="A2"><label>b</label>Cancer Research UK, Viral Oncology group, UCL Cancer Institute, London, England</aff><author-notes><corresp id="FN1"><label>*</label>Correspondence to: Department of Microbiology, University of Washington, Box 357735, Seattle, WA, USA. Fax: +1 206 543 8297. <email>lagunoff@u.washington.edu</email> (M. Lagunoff)</corresp></author-notes><pub-date pub-type="nihms-submitted"><day>21</day><month>11</month><year>2012</year></pub-date><pub-date pub-type="epub"><day>21</day><month>4</month><year>2012</year></pub-date><pub-date pub-type="ppub"><day>5</day><month>7</month><year>2012</year></pub-date><pub-date pub-type="pmc-release"><day>05</day><month>7</month><year>2013</year></pub-date><volume>428</volume><issue>2</issue><fpage>112</fpage><lpage>120</lpage><permissions><copyright-statement>© 2012 Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2012</copyright-year></permissions><abstract><p id="P1">The predominant tumor cell of Kaposi’s Sarcoma (KS) is the spindle cell, a cell of endothelial origin that expresses markers of lymphatic endothelium. In culture, Kaposi’s Sarcoma-associated herpesvirus (KSHV) infection of blood endothelial cells drives expression of lymphatic endothelial cell specific markers, in a process that requires activation of the gp130 receptor and the JAK2/STAT3 and PI3K/AKT signaling pathways. While expression of each of the KSHV major latent genes in endothelial cells failed to increase expression of lymphatic markers, the viral homolog of human IL-6 (vIL-6) was sufficient for induction and requires the JAK2/STAT3 and PI3K/AKT pathways. Therefore, activation of gp130 and downstream signaling by vIL-6 is sufficient to drive blood to lymphatic endothelial cell differentiation. While sufficient, vIL-6 is not necessary for lymphatic reprogramming in the context of viral infection. This indicates that multiple viral genes are involved and suggests a central importance of this pathway to KSHV pathogenesis.</p></abstract><kwd-group><kwd>KSHV</kwd><kwd>HHV-8</kwd><kwd>Kaposi’s Sarcoma</kwd><kwd>vIL-6</kwd><kwd>Lymphatic endothelial cells</kwd><kwd>Lymphatic endothelial cell differentiation</kwd></kwd-group><funding-group><award-group><funding-source country="United States">National Cancer Institute : NCI</funding-source><award-id>R01 CA097934 || CA</award-id></award-group><award-group><funding-source country="United States">National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID</funding-source><award-id>P30 AI027757 || AI</award-id></award-group></funding-group></article-meta></front></pmc><affiliations><list><country><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><country name="États-Unis"><region name="Washington (État)"><name sortKey="Morris, Valerie A" sort="Morris, Valerie A" uniqKey="Morris V" first="Valerie A." last="Morris">Valerie A. Morris</name></region><name sortKey="Lagunoff, Michael" sort="Lagunoff, Michael" uniqKey="Lagunoff M" first="Michael" last="Lagunoff">Michael Lagunoff</name><name sortKey="Punjabi, Almira S" sort="Punjabi, Almira S" uniqKey="Punjabi A" first="Almira S." last="Punjabi">Almira S. Punjabi</name><name sortKey="Wells, Robert C" sort="Wells, Robert C" uniqKey="Wells R" first="Robert C." last="Wells">Robert C. Wells</name><name sortKey="Wittkopp, Cristina J" sort="Wittkopp, Cristina J" uniqKey="Wittkopp C" first="Cristina J." last="Wittkopp">Cristina J. Wittkopp</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Vart, Richard" sort="Vart, Richard" uniqKey="Vart R" first="Richard" last="Vart">Richard Vart</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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