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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Tie1 is required for lymphatic valve and collecting vessel development</title><author><name sortKey="Qu, Xianghu" sort="Qu, Xianghu" uniqKey="Qu X" first="Xianghu" last="Qu">Xianghu Qu</name><affiliation><nlm:aff id="A1"> Department of Pediatrics (Cardiology), Vanderbilt University Medical Center, Nashville, TN 37232, USA.</nlm:aff></affiliation></author><author><name sortKey="Zhou, Bin" sort="Zhou, Bin" uniqKey="Zhou B" first="Bin" last="Zhou">Bin Zhou</name><affiliation><nlm:aff id="A3"> Department of Genetics, Albert Einstein College of Medicine, NY 10461, USA.</nlm:aff></affiliation></author><author><name sortKey="Baldwin, H Scott" sort="Baldwin, H Scott" uniqKey="Baldwin H" first="H. Scott" last="Baldwin">H. Scott Baldwin</name><affiliation><nlm:aff id="A1"> Department of Pediatrics (Cardiology), Vanderbilt University Medical Center, Nashville, TN 37232, USA.</nlm:aff></affiliation><affiliation><nlm:aff id="A2"> Department of Cell and Development Biology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25576926</idno><idno type="pmc">4374493</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4374493</idno><idno type="RBID">PMC:4374493</idno><idno type="doi">10.1016/j.ydbio.2014.12.021</idno><date when="2015">2015</date><idno type="wicri:Area/Pmc/Corpus">003356</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">003356</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Tie1 is required for lymphatic valve and collecting vessel development</title><author><name sortKey="Qu, Xianghu" sort="Qu, Xianghu" uniqKey="Qu X" first="Xianghu" last="Qu">Xianghu Qu</name><affiliation><nlm:aff id="A1"> Department of Pediatrics (Cardiology), Vanderbilt University Medical Center, Nashville, TN 37232, USA.</nlm:aff></affiliation></author><author><name sortKey="Zhou, Bin" sort="Zhou, Bin" uniqKey="Zhou B" first="Bin" last="Zhou">Bin Zhou</name><affiliation><nlm:aff id="A3"> Department of Genetics, Albert Einstein College of Medicine, NY 10461, USA.</nlm:aff></affiliation></author><author><name sortKey="Baldwin, H Scott" sort="Baldwin, H Scott" uniqKey="Baldwin H" first="H. Scott" last="Baldwin">H. Scott Baldwin</name><affiliation><nlm:aff id="A1"> Department of Pediatrics (Cardiology), Vanderbilt University Medical Center, Nashville, TN 37232, USA.</nlm:aff></affiliation><affiliation><nlm:aff id="A2"> Department of Cell and Development Biology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.</nlm:aff></affiliation></author></analytic><series><title level="j">Developmental biology</title><idno type="ISSN">0012-1606</idno><idno type="eISSN">1095-564X</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Tie1 is a receptor tyrosine kinase with broad expression in embryonic endothelium. Reduction of Tie1 levels in mouse embryos with a hypomorphic Tie1 allele resulted in abnormal lymphatic patterning and architecture, decreased lymphatic draining efficiency, and ultimately, embryonic demise. Here we report that Tie1 is present uniformly throughout the lymphatics and from late embryonic/early postnatal stages, becomes more restricted to lymphatic valve regions. To investigate later events of lymphatic development, we employed Cre-<italic>loxP</italic> recombination utilizing a floxed <italic>Tie1</italic> allele and an <italic>Nfatc1Cre</italic> line, to provide <italic>loxP</italic> excision predominantly in lymphatic endothelium and developing valves. Interestingly, unlike the early prenatal defects previously described by ubiquitous endothelial deletion, excision of <italic>Tie1</italic> with <italic>Nfatc1Cre</italic> resulted in abnormal lymphatic defects in postnatal mice and was characterized by agenesis of lymphatic valves and a deficiency of collecting lymphatic vessels. Attenuation of Tie1 signaling in lymphatic endothelium prevented initiation of lymphatic valve specification by Prox1 high expression lymphatic endothelial cells that is associated with the onset of turbulent flow in the lymphatic circulation. Our findings reveal a fundamental role for Tie signaling during lymphatic vessel remodeling and valve morphogenesis and implicate it as a candidate gene involved in primary lymphedema.</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">0372762</journal-id><journal-id journal-id-type="pubmed-jr-id">3389</journal-id><journal-id journal-id-type="nlm-ta">Dev Biol</journal-id><journal-id journal-id-type="iso-abbrev">Dev. Biol.</journal-id><journal-title-group><journal-title>Developmental biology</journal-title></journal-title-group><issn pub-type="ppub">0012-1606</issn><issn pub-type="epub">1095-564X</issn></journal-meta><article-meta><article-id pub-id-type="pmid">25576926</article-id><article-id pub-id-type="pmc">4374493</article-id><article-id pub-id-type="doi">10.1016/j.ydbio.2014.12.021</article-id><article-id pub-id-type="manuscript">NIHMS653687</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Tie1 is required for lymphatic valve and collecting vessel development</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Qu</surname><given-names>Xianghu</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Zhou</surname><given-names>Bin</given-names></name><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Baldwin</surname><given-names>H. Scott</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib></contrib-group><aff id="A1"><label>1</label> Department of Pediatrics (Cardiology), Vanderbilt University Medical Center, Nashville, TN 37232, USA.</aff><aff id="A2"><label>2</label> Department of Cell and Development Biology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.</aff><aff id="A3"><label>3</label> Department of Genetics, Albert Einstein College of Medicine, NY 10461, USA.</aff><author-notes><corresp id="CR1"><bold>Correspondence:</bold> H. Scott Baldwin, M.D. Division of Pediatric Cardiology Vanderbilt University Medical Center 9435-A MRB IV-Langford 2213 Garland Ave. Nashville, TN 37232-0493 Ph: 615.322.2703 Fax: 615.322.6541 <email>scott.baldwin@vanderbilt.edu</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>27</day><month>2</month><year>2015</year></pub-date><pub-date pub-type="epub"><day>07</day><month>1</month><year>2015</year></pub-date><pub-date pub-type="ppub"><day>1</day><month>3</month><year>2015</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>3</month><year>2016</year></pub-date><volume>399</volume><issue>1</issue><fpage>117</fpage><lpage>128</lpage><pmc-comment>elocation-id from pubmed: 10.1016/j.ydbio.2014.12.021</pmc-comment>
<permissions><copyright-statement>© 2015 Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2015</copyright-year></permissions><abstract><p id="P1">Tie1 is a receptor tyrosine kinase with broad expression in embryonic endothelium. Reduction of Tie1 levels in mouse embryos with a hypomorphic Tie1 allele resulted in abnormal lymphatic patterning and architecture, decreased lymphatic draining efficiency, and ultimately, embryonic demise. Here we report that Tie1 is present uniformly throughout the lymphatics and from late embryonic/early postnatal stages, becomes more restricted to lymphatic valve regions. To investigate later events of lymphatic development, we employed Cre-<italic>loxP</italic> recombination utilizing a floxed <italic>Tie1</italic> allele and an <italic>Nfatc1Cre</italic> line, to provide <italic>loxP</italic> excision predominantly in lymphatic endothelium and developing valves. Interestingly, unlike the early prenatal defects previously described by ubiquitous endothelial deletion, excision of <italic>Tie1</italic> with <italic>Nfatc1Cre</italic> resulted in abnormal lymphatic defects in postnatal mice and was characterized by agenesis of lymphatic valves and a deficiency of collecting lymphatic vessels. Attenuation of Tie1 signaling in lymphatic endothelium prevented initiation of lymphatic valve specification by Prox1 high expression lymphatic endothelial cells that is associated with the onset of turbulent flow in the lymphatic circulation. Our findings reveal a fundamental role for Tie signaling during lymphatic vessel remodeling and valve morphogenesis and implicate it as a candidate gene involved in primary lymphedema.</p></abstract><kwd-group><kwd>Tie1</kwd><kwd>lymphatic valve</kwd><kwd>lymphovenous valve</kwd><kwd>lymphatic vessel remodeling</kwd><kwd>conditional knockout</kwd><kwd>Prox1</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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