The KSHV viral IL-6 homolog is sufficient to induce blood to lymphatic endothelial cell differentiation
Identifieur interne : 003E30 ( Main/Exploration ); précédent : 003E29; suivant : 003E31The 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
Affiliations:
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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. 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Wittkopp</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="Vart, Richard" sort="Vart, Richard" uniqKey="Vart R" first="Richard" last="Vart">Richard Vart</name><affiliation wicri:level="2"><nlm:aff id="A2">Cancer Research UK, Viral Oncology group, UCL Cancer Institute, London, England</nlm:aff><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Cancer Research UK, Viral Oncology group, UCL Cancer Institute, London</wicri:cityArea></affiliation></author><author><name sortKey="Lagunoff, Michael" sort="Lagunoff, Michael" uniqKey="Lagunoff M" first="Michael" last="Lagunoff">Michael Lagunoff</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></analytic><series><title level="j">Virology</title><idno type="ISSN">0042-6822</idno><idno type="eISSN">1096-0341</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><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></div></front></TEI><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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