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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">HIF-1α coordinates lymphangiogenesis during wound healing and in response to inflammation</title><author><name sortKey="Zampell, Jamie C" sort="Zampell, Jamie C" uniqKey="Zampell J" first="Jamie C." last="Zampell">Jamie C. Zampell</name></author><author><name sortKey="Yan, Alan" sort="Yan, Alan" uniqKey="Yan A" first="Alan" last="Yan">Alan Yan</name></author><author><name sortKey="Avraham, Tomer" sort="Avraham, Tomer" uniqKey="Avraham T" first="Tomer" last="Avraham">Tomer Avraham</name></author><author><name sortKey="Daluvoy, Sanjay" sort="Daluvoy, Sanjay" uniqKey="Daluvoy S" first="Sanjay" last="Daluvoy">Sanjay Daluvoy</name></author><author><name sortKey="Weitman, Evan S" sort="Weitman, Evan S" uniqKey="Weitman E" first="Evan S." last="Weitman">Evan S. Weitman</name></author><author><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J." last="Mehrara">Babak J. Mehrara</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22067482</idno><idno type="pmc">3470728</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3470728</idno><idno type="RBID">PMC:3470728</idno><idno type="doi">10.1096/fj.11-195321</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">002E00</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">002E00</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">HIF-1α coordinates lymphangiogenesis during wound healing and in response to inflammation</title><author><name sortKey="Zampell, Jamie C" sort="Zampell, Jamie C" uniqKey="Zampell J" first="Jamie C." last="Zampell">Jamie C. Zampell</name></author><author><name sortKey="Yan, Alan" sort="Yan, Alan" uniqKey="Yan A" first="Alan" last="Yan">Alan Yan</name></author><author><name sortKey="Avraham, Tomer" sort="Avraham, Tomer" uniqKey="Avraham T" first="Tomer" last="Avraham">Tomer Avraham</name></author><author><name sortKey="Daluvoy, Sanjay" sort="Daluvoy, Sanjay" uniqKey="Daluvoy S" first="Sanjay" last="Daluvoy">Sanjay Daluvoy</name></author><author><name sortKey="Weitman, Evan S" sort="Weitman, Evan S" uniqKey="Weitman E" first="Evan S." last="Weitman">Evan S. Weitman</name></author><author><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J." last="Mehrara">Babak J. Mehrara</name></author></analytic><series><title level="j">The FASEB Journal</title><idno type="ISSN">0892-6638</idno><idno type="eISSN">1530-6860</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>This study aimed to investigate the mechanisms that coordinate lymphangiogenesis. Using mouse models of lymphatic regeneration and inflammatory lymphangiogenesis, we explored the hypothesis that hypoxia inducible factor-α (HIF-1α) is a central regulator of lymphangiogenesis. We show that HIF-1α inhibition by small molecule inhibitors (YC-1 and 2-methyoxyestradiol) results in delayed lymphatic repair, decreased local vascular endothelial growth factor-C (VEGF-C) expression, reduced numbers of VEGF-C<sup>+</sup> cells, and reductions in inflammatory lymphangiogenesis. Using transgenic HIF-1α/luciferase mice to image HIF-1α expression in real time in addition to Western blot analysis and pimonidazole staining for cellular hypoxia, we demonstrate that hypoxia stabilizes HIF-1α during initial stages of wound repair (1–2 wk); whereas inflammation secondary to gradients of lymphatic fluid stasis stabilizes HIF-1α thereafter (3–6 wk). In addition, we show that CD4<sup>+</sup> cell-mediated inflammation is necessary for this response and regulates HIF-1α expression by macrophages, as CD4-deficient or CD4-depleted mice demonstrate 2-fold reductions in HIF-1α expression as compared to wild-types. In summary, we show that HIF-1α is a critical coordinator of lymphangiogenesis by regulating the expression of lymphangiogenic cytokines as part of an early response mechanism to hypoxia, inflammation, and lymphatic fluid stasis.—Zampell, J. C., Yan, A., Avraham, T., Daluvoy, S., Weitman, E. S., Mehrara, B. J. HIF-1α coordinates lymphangiogenesis during wound healing and in response to inflammation.</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>
<front><journal-meta><journal-id journal-id-type="nlm-ta">FASEB J</journal-id><journal-id journal-id-type="iso-abbrev">FASEB J</journal-id><journal-id journal-id-type="hwp">fasebj</journal-id><journal-id journal-id-type="pmc">fasebj</journal-id><journal-id journal-id-type="publisher-id">FASEB</journal-id><journal-title-group><journal-title>The FASEB Journal</journal-title></journal-title-group><issn pub-type="ppub">0892-6638</issn><issn pub-type="epub">1530-6860</issn><publisher><publisher-name>Federation of American Societies for Experimental Biology</publisher-name><publisher-loc>Bethesda, MD, USA</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">22067482</article-id><article-id pub-id-type="pmc">3470728</article-id><article-id pub-id-type="publisher-id">11-195321</article-id><article-id pub-id-type="doi">10.1096/fj.11-195321</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Communications</subject></subj-group></article-categories><title-group><article-title>HIF-1α coordinates lymphangiogenesis during wound healing and in response to inflammation</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Zampell</surname><given-names>Jamie C.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Yan</surname><given-names>Alan</given-names></name></contrib><contrib contrib-type="author"><name><surname>Avraham</surname><given-names>Tomer</given-names></name></contrib><contrib contrib-type="author"><name><surname>Daluvoy</surname><given-names>Sanjay</given-names></name></contrib><contrib contrib-type="author"><name><surname>Weitman</surname><given-names>Evan S.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Mehrara</surname><given-names>Babak J.</given-names></name><xref ref-type="corresp" rid="cor1"><sup>1</sup></xref></contrib><aff>Division of Plastic and Reconstructive Surgery and Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York, USA</aff></contrib-group><author-notes><corresp id="cor1"><label>1</label> Correspondence: <addr-line>Memorial Sloan-Kettering Cancer Center, 1275 York Ave., Rm. MRI 1005, New York, NY 10065, USA</addr-line>. E-mail: <email>mehrarab@mskcc.org</email></corresp></author-notes><pub-date pub-type="ppub"><month>3</month><year>2012</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>3</month><year>2013</year></pub-date><pmc-comment> PMC Release delay is 12 months and 0 days and was based on the
<volume>26</volume><issue>3</issue><fpage>1027</fpage><lpage>1039</lpage><history><date date-type="received"><day>1</day><month>9</month><year>2011</year></date><date date-type="accepted"><day>1</day><month>11</month><year>2011</year></date></history><permissions><copyright-statement>© FASEB</copyright-statement><copyright-year>2012</copyright-year></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="z3800312001027.pdf"></self-uri><abstract><p>This study aimed to investigate the mechanisms that coordinate lymphangiogenesis. Using mouse models of lymphatic regeneration and inflammatory lymphangiogenesis, we explored the hypothesis that hypoxia inducible factor-α (HIF-1α) is a central regulator of lymphangiogenesis. We show that HIF-1α inhibition by small molecule inhibitors (YC-1 and 2-methyoxyestradiol) results in delayed lymphatic repair, decreased local vascular endothelial growth factor-C (VEGF-C) expression, reduced numbers of VEGF-C<sup>+</sup> cells, and reductions in inflammatory lymphangiogenesis. Using transgenic HIF-1α/luciferase mice to image HIF-1α expression in real time in addition to Western blot analysis and pimonidazole staining for cellular hypoxia, we demonstrate that hypoxia stabilizes HIF-1α during initial stages of wound repair (1–2 wk); whereas inflammation secondary to gradients of lymphatic fluid stasis stabilizes HIF-1α thereafter (3–6 wk). In addition, we show that CD4<sup>+</sup> cell-mediated inflammation is necessary for this response and regulates HIF-1α expression by macrophages, as CD4-deficient or CD4-depleted mice demonstrate 2-fold reductions in HIF-1α expression as compared to wild-types. In summary, we show that HIF-1α is a critical coordinator of lymphangiogenesis by regulating the expression of lymphangiogenic cytokines as part of an early response mechanism to hypoxia, inflammation, and lymphatic fluid stasis.—Zampell, J. C., Yan, A., Avraham, T., Daluvoy, S., Weitman, E. S., Mehrara, B. J. HIF-1α coordinates lymphangiogenesis during wound healing and in response to inflammation.</p></abstract><kwd-group><kwd>hypoxia inducible factor-1α</kwd><kwd>CD4 cells</kwd><kwd>hypoxia</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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