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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pentraxin-3 Is a TSH-Inducible Protein in Human Fibrocytes and Orbital Fibroblasts</title><author><name sortKey="Wang, Hao" sort="Wang, Hao" uniqKey="Wang H" first="Hao" last="Wang">Hao Wang</name></author><author><name sortKey="Atkins, Stephen J" sort="Atkins, Stephen J" uniqKey="Atkins S" first="Stephen J." last="Atkins">Stephen J. Atkins</name></author><author><name sortKey="Fernando, Roshini" sort="Fernando, Roshini" uniqKey="Fernando R" first="Roshini" last="Fernando">Roshini Fernando</name></author><author><name sortKey="Wei, Rui Li" sort="Wei, Rui Li" uniqKey="Wei R" first="Rui-Li" last="Wei">Rui-Li Wei</name></author><author><name sortKey="Smith, Terry J" sort="Smith, Terry J" uniqKey="Smith T" first="Terry J." last="Smith">Terry J. Smith</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">26287404</idno><idno type="pmc">4606754</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4606754</idno><idno type="RBID">PMC:4606754</idno><idno type="doi">10.1210/en.2015-1399</idno><date when="2015">2015</date><idno type="wicri:Area/Pmc/Corpus">000265</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000265</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Pentraxin-3 Is a TSH-Inducible Protein in Human Fibrocytes and Orbital Fibroblasts</title><author><name sortKey="Wang, Hao" sort="Wang, Hao" uniqKey="Wang H" first="Hao" last="Wang">Hao Wang</name></author><author><name sortKey="Atkins, Stephen J" sort="Atkins, Stephen J" uniqKey="Atkins S" first="Stephen J." last="Atkins">Stephen J. Atkins</name></author><author><name sortKey="Fernando, Roshini" sort="Fernando, Roshini" uniqKey="Fernando R" first="Roshini" last="Fernando">Roshini Fernando</name></author><author><name sortKey="Wei, Rui Li" sort="Wei, Rui Li" uniqKey="Wei R" first="Rui-Li" last="Wei">Rui-Li Wei</name></author><author><name sortKey="Smith, Terry J" sort="Smith, Terry J" uniqKey="Smith T" first="Terry J." last="Smith">Terry J. Smith</name></author></analytic><series><title level="j">Endocrinology</title><idno type="ISSN">0013-7227</idno><idno type="eISSN">1945-7170</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>CD34<sup>+</sup> fibrocytes are bone marrow–derived monocyte progenitor cells that traffic to sites of tissue injury and repair. They putatively infiltrate the orbit in thyroid-associated ophthalmopathy where they appear to transition into CD34<sup>+</sup> orbital fibroblasts (OFs) that interact with residential CD34<sup>−</sup> fibroblasts. A unique phenotypic attribute of fibrocytes and CD34<sup>+</sup> OFs is their expression of the functional thyrotropin receptor (TSHR) and other “thyroid-specific” proteins. When activated through TSHR, fibrocytes express a number of cytokines and other inflammatory genes. Here we sought to determine whether pentraxin-3 (PTX-3), an acute-phase protein involved in inflammation and autoimmunity, might be induced by TSH in fibrocytes and OFs. These cells were collected from patients with Graves disease and healthy individuals. PTX-3 mRNA levels were determined by real-time PCR, protein was determined by ELISA and Western blot, and PTX-3 gene promoter activity was assessed with reporter assays. PTX-3 expression was induced by TSH in both cell types, regardless of the health status of the donor and was a consequence of increased steady-state PTX-3 mRNA levels. M22, a TSHR-activating monoclonal antibody, also induced PTX-3. The induction could be attenuated by dexamethasone and by IGF-I receptor–blocking antibodies, teprotumumab and 1H7. TSH effects were mediated through phosphatidylinositol 3-kinase/AKT, mammalian target of rapamycin/p70<sup>s6k</sup>, Janus tyrosine kinase 2 pathways, and enhanced PTX-3 mRNA stability. These findings indicate that PTX-3 is a TSH target gene, the expression of which can be induced in fibrocytes and OFs. They suggest that PTX-3 might represent a previously unidentified nexus between the thyroid axis and the mechanisms involved in tissue remodeling.</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">Endocrinology</journal-id><journal-id journal-id-type="iso-abbrev">Endocrinology</journal-id><journal-id journal-id-type="hwp">endo</journal-id><journal-id journal-id-type="publisher-id">endoc</journal-id><journal-id journal-id-type="pmc">endo</journal-id><journal-title-group><journal-title>Endocrinology</journal-title></journal-title-group><issn pub-type="ppub">0013-7227</issn><issn pub-type="epub">1945-7170</issn><publisher><publisher-name>Endocrine Society</publisher-name><publisher-loc>Washington, DC</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26287404</article-id><article-id pub-id-type="pmc">4606754</article-id><article-id pub-id-type="publisher-id">EN-15-1399</article-id><article-id pub-id-type="doi">10.1210/en.2015-1399</article-id><article-categories><subj-group subj-group-type="heading"><subject>Original Research</subject><subj-group><subject>Thyroid-TRH-TSH</subject></subj-group></subj-group></article-categories><title-group><article-title>Pentraxin-3 Is a TSH-Inducible Protein in Human Fibrocytes and Orbital Fibroblasts</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Hao</given-names></name></contrib><contrib contrib-type="author"><name><surname>Atkins</surname><given-names>Stephen J.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Fernando</surname><given-names>Roshini</given-names></name></contrib><contrib contrib-type="author"><name><surname>Wei</surname><given-names>Rui-Li</given-names></name></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Smith</surname><given-names>Terry J.</given-names></name></contrib><aff>Departments of Ophthalmology and Visual Sciences (H.W., S.J.A., R.F., T.J.S.), University of Michigan Medical School, Ann Arbor, Michigan 48105; Department of Ophthalmology (H.W., R.-L.W.), Shanghai Changzheng Hospital, Second Military Medical University, 200003 Shanghai, China; and Division of Metabolism (T.J.S.), Endocrinology, and Diabetes, University of Michigan Medical School, Ann Arbor, Michigan 48105</aff></contrib-group><author-notes><corresp>Address all correspondence and requests for reprints to: Terry J. Smith, MD, <addr-line>Department of Ophthalmology and Visual Sciences, University of Michigan Medical School, Kellogg Eye Center, Brehm Tower, 1000 Wall Street, Ann Arbor, MI 48105.</addr-line> E-mail: <email>terrysmi@med.umich.edu</email>.</corresp></author-notes><pub-date pub-type="ppub"><month>11</month><year>2015</year></pub-date><pub-date pub-type="epub"><day>19</day><month>8</month><year>2015</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>11</month><year>2016</year></pub-date><pmc-comment> PMC Release delay is 12 months and
0 days and was based on the
<volume>156</volume><issue>11</issue><fpage>4336</fpage><lpage>4344</lpage><history><date date-type="received"><day>5</day><month>5</month><year>2015</year></date><date date-type="accepted"><day>13</day><month>8</month><year>2015</year></date></history><permissions><copyright-statement>Copyright © 2015 by the Endocrine Society</copyright-statement><copyright-year>2015</copyright-year></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zee01115004336.pdf"></self-uri><abstract><p>CD34<sup>+</sup> fibrocytes are bone marrow–derived monocyte progenitor cells that traffic to sites of tissue injury and repair. They putatively infiltrate the orbit in thyroid-associated ophthalmopathy where they appear to transition into CD34<sup>+</sup> orbital fibroblasts (OFs) that interact with residential CD34<sup>−</sup> fibroblasts. A unique phenotypic attribute of fibrocytes and CD34<sup>+</sup> OFs is their expression of the functional thyrotropin receptor (TSHR) and other “thyroid-specific” proteins. When activated through TSHR, fibrocytes express a number of cytokines and other inflammatory genes. Here we sought to determine whether pentraxin-3 (PTX-3), an acute-phase protein involved in inflammation and autoimmunity, might be induced by TSH in fibrocytes and OFs. These cells were collected from patients with Graves disease and healthy individuals. PTX-3 mRNA levels were determined by real-time PCR, protein was determined by ELISA and Western blot, and PTX-3 gene promoter activity was assessed with reporter assays. PTX-3 expression was induced by TSH in both cell types, regardless of the health status of the donor and was a consequence of increased steady-state PTX-3 mRNA levels. M22, a TSHR-activating monoclonal antibody, also induced PTX-3. The induction could be attenuated by dexamethasone and by IGF-I receptor–blocking antibodies, teprotumumab and 1H7. TSH effects were mediated through phosphatidylinositol 3-kinase/AKT, mammalian target of rapamycin/p70<sup>s6k</sup>, Janus tyrosine kinase 2 pathways, and enhanced PTX-3 mRNA stability. These findings indicate that PTX-3 is a TSH target gene, the expression of which can be induced in fibrocytes and OFs. They suggest that PTX-3 might represent a previously unidentified nexus between the thyroid axis and the mechanisms involved in tissue remodeling.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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