TGF-beta promotes thyroid epithelial cell hyperplasia and fibrosis in IFN-gamma-deficient NOD.H-2h4 mice
IFN-gamma(-/-)NOD.H-2h4 mice given 0.05% NaI in their water develop severe thyroid epithelial cell (thyrocyte) hyperplasia and proliferation (TEC H/P) and fibrosis. Proliferating thyrocytes of IFN-gamma(-/-) mice with TEC H/P produce TGF-beta as demonstrated by immunohistochemical staining and in si...
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| Veröffentlicht in: | The Journal of immunology (1950) 2008-08, Vol.181 (3), p.2238-2245 |
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| container_title | The Journal of immunology (1950) |
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| creator | Yu, Shiguang Sharp, Gordon C Braley-Mullen, Helen |
| description | IFN-gamma(-/-)NOD.H-2h4 mice given 0.05% NaI in their water develop severe thyroid epithelial cell (thyrocyte) hyperplasia and proliferation (TEC H/P) and fibrosis. Proliferating thyrocytes of IFN-gamma(-/-) mice with TEC H/P produce TGF-beta as demonstrated by immunohistochemical staining and in situ hybridization. Strong expression of activating phosphorylated Smad-2/3 and weak expression of inhibitory Smad-7 by proliferating thyrocytes correlate with the severity of TEC H/P. Splenocytes from IFN-gamma(-/-) mice with severe TEC H/P transfer severe TEC H/P to IFN-gamma(-/-)NOD.H-2h4.SCID mice. Mice given anti-TGF-beta had markedly reduced thyrocyte proliferation and decreased fibrosis compared with mouse Ig-treated controls, suggesting that TGF-beta plays an important role in development of TEC H/P induced by activated splenocytes. Moreover, transgenic IFN-gamma(-/-)NOD.H-2h4 mice expressing TGF-beta on thyrocytes all develop fibrosis and moderate to severe TEC H/P with accelerated kinetics, directly demonstrating a role for TGF-beta in severe TEC H/P and fibrosis. |
| doi_str_mv | 10.4049/jimmunol.181.3.2238 |
| format | Article |
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Proliferating thyrocytes of IFN-gamma(-/-) mice with TEC H/P produce TGF-beta as demonstrated by immunohistochemical staining and in situ hybridization. Strong expression of activating phosphorylated Smad-2/3 and weak expression of inhibitory Smad-7 by proliferating thyrocytes correlate with the severity of TEC H/P. Splenocytes from IFN-gamma(-/-) mice with severe TEC H/P transfer severe TEC H/P to IFN-gamma(-/-)NOD.H-2h4.SCID mice. Mice given anti-TGF-beta had markedly reduced thyrocyte proliferation and decreased fibrosis compared with mouse Ig-treated controls, suggesting that TGF-beta plays an important role in development of TEC H/P induced by activated splenocytes. Moreover, transgenic IFN-gamma(-/-)NOD.H-2h4 mice expressing TGF-beta on thyrocytes all develop fibrosis and moderate to severe TEC H/P with accelerated kinetics, directly demonstrating a role for TGF-beta in severe TEC H/P and fibrosis.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.181.3.2238</identifier><identifier>PMID: 18641364</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Antibodies - immunology ; Cell Proliferation ; Epithelial Cells - cytology ; Epithelial Cells - metabolism ; Fibrosis - genetics ; Fibrosis - metabolism ; Fibrosis - pathology ; Interferon-gamma - deficiency ; Interferon-gamma - genetics ; Interferon-gamma - metabolism ; Mice ; Mice, Inbred NOD ; Mice, Knockout ; Phosphorylation ; Protein-Serine-Threonine Kinases - metabolism ; Receptor, Transforming Growth Factor-beta Type II ; Receptors, Transforming Growth Factor beta - metabolism ; Smad2 Protein - metabolism ; Smad3 Protein - metabolism ; Spleen - immunology ; Spleen - metabolism ; Thymus Hyperplasia - genetics ; Thymus Hyperplasia - metabolism ; Thymus Hyperplasia - pathology ; Transforming Growth Factor beta - genetics ; Transforming Growth Factor beta - immunology ; Transforming Growth Factor beta - metabolism</subject><ispartof>The Journal of immunology (1950), 2008-08, Vol.181 (3), p.2238-2245</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c348t-2952a6258a815138d9c9a4e83df922ea2b783427defae80ac0f726c29c5ebe243</citedby><cites>FETCH-LOGICAL-c348t-2952a6258a815138d9c9a4e83df922ea2b783427defae80ac0f726c29c5ebe243</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18641364$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Shiguang</creatorcontrib><creatorcontrib>Sharp, Gordon C</creatorcontrib><creatorcontrib>Braley-Mullen, Helen</creatorcontrib><title>TGF-beta promotes thyroid epithelial cell hyperplasia and fibrosis in IFN-gamma-deficient NOD.H-2h4 mice</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>IFN-gamma(-/-)NOD.H-2h4 mice given 0.05% NaI in their water develop severe thyroid epithelial cell (thyrocyte) hyperplasia and proliferation (TEC H/P) and fibrosis. Proliferating thyrocytes of IFN-gamma(-/-) mice with TEC H/P produce TGF-beta as demonstrated by immunohistochemical staining and in situ hybridization. Strong expression of activating phosphorylated Smad-2/3 and weak expression of inhibitory Smad-7 by proliferating thyrocytes correlate with the severity of TEC H/P. Splenocytes from IFN-gamma(-/-) mice with severe TEC H/P transfer severe TEC H/P to IFN-gamma(-/-)NOD.H-2h4.SCID mice. Mice given anti-TGF-beta had markedly reduced thyrocyte proliferation and decreased fibrosis compared with mouse Ig-treated controls, suggesting that TGF-beta plays an important role in development of TEC H/P induced by activated splenocytes. Moreover, transgenic IFN-gamma(-/-)NOD.H-2h4 mice expressing TGF-beta on thyrocytes all develop fibrosis and moderate to severe TEC H/P with accelerated kinetics, directly demonstrating a role for TGF-beta in severe TEC H/P and fibrosis.</description><subject>Animals</subject><subject>Antibodies - immunology</subject><subject>Cell Proliferation</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial Cells - metabolism</subject><subject>Fibrosis - genetics</subject><subject>Fibrosis - metabolism</subject><subject>Fibrosis - pathology</subject><subject>Interferon-gamma - deficiency</subject><subject>Interferon-gamma - genetics</subject><subject>Interferon-gamma - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>Mice, Knockout</subject><subject>Phosphorylation</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Receptor, Transforming Growth Factor-beta Type II</subject><subject>Receptors, Transforming Growth Factor beta - metabolism</subject><subject>Smad2 Protein - metabolism</subject><subject>Smad3 Protein - metabolism</subject><subject>Spleen - immunology</subject><subject>Spleen - metabolism</subject><subject>Thymus Hyperplasia - genetics</subject><subject>Thymus Hyperplasia - metabolism</subject><subject>Thymus Hyperplasia - pathology</subject><subject>Transforming Growth Factor beta - genetics</subject><subject>Transforming Growth Factor beta - immunology</subject><subject>Transforming Growth Factor beta - metabolism</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkLtOwzAUhi0EgnJ5AiTkic3BtzjOiAq9SBVdymw5zgkxipMQp0PfnlQtYjrLfzn_h9Ajo4mkMn_59iHs265JmGaJSDgX-gLNWJpSohRVl2hGKeeEZSq7QbcxflNKFeXyGt0wrSQTSs5QvVsuSAGjxf3QhW6EiMf6MHS-xND7sYbG2wY7aBpcH3oY-sZGb7FtS1z5Yuiij9i3eL34IF82BEtKqLzz0I74Y_uWrAivJQ7ewT26qmwT4eF879Dn4n03X5HNdrmev26IE1KPhOcpt4qn2mqWMqHL3OVWghZllXMOlheZFpJnU40FTa2jVcaV47lLoQAuxR16PuVOe372EEcTfDz-b1vo9tGoXAjBRDYJxUnophVxgMr0gw92OBhGzRGw-QNsJsBGmCPgyfV0jt8XAcp_z5mo-AWgS3kU</recordid><startdate>20080801</startdate><enddate>20080801</enddate><creator>Yu, Shiguang</creator><creator>Sharp, Gordon C</creator><creator>Braley-Mullen, Helen</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20080801</creationdate><title>TGF-beta promotes thyroid epithelial cell hyperplasia and fibrosis in IFN-gamma-deficient NOD.H-2h4 mice</title><author>Yu, Shiguang ; Sharp, Gordon C ; Braley-Mullen, Helen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c348t-2952a6258a815138d9c9a4e83df922ea2b783427defae80ac0f726c29c5ebe243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Antibodies - immunology</topic><topic>Cell Proliferation</topic><topic>Epithelial Cells - cytology</topic><topic>Epithelial Cells - metabolism</topic><topic>Fibrosis - genetics</topic><topic>Fibrosis - metabolism</topic><topic>Fibrosis - pathology</topic><topic>Interferon-gamma - deficiency</topic><topic>Interferon-gamma - genetics</topic><topic>Interferon-gamma - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Mice, Knockout</topic><topic>Phosphorylation</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Receptor, Transforming Growth Factor-beta Type II</topic><topic>Receptors, Transforming Growth Factor beta - metabolism</topic><topic>Smad2 Protein - metabolism</topic><topic>Smad3 Protein - metabolism</topic><topic>Spleen - immunology</topic><topic>Spleen - metabolism</topic><topic>Thymus Hyperplasia - genetics</topic><topic>Thymus Hyperplasia - metabolism</topic><topic>Thymus Hyperplasia - pathology</topic><topic>Transforming Growth Factor beta - genetics</topic><topic>Transforming Growth Factor beta - immunology</topic><topic>Transforming Growth Factor beta - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Shiguang</creatorcontrib><creatorcontrib>Sharp, Gordon C</creatorcontrib><creatorcontrib>Braley-Mullen, Helen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Shiguang</au><au>Sharp, Gordon C</au><au>Braley-Mullen, Helen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TGF-beta promotes thyroid epithelial cell hyperplasia and fibrosis in IFN-gamma-deficient NOD.H-2h4 mice</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2008-08-01</date><risdate>2008</risdate><volume>181</volume><issue>3</issue><spage>2238</spage><epage>2245</epage><pages>2238-2245</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>IFN-gamma(-/-)NOD.H-2h4 mice given 0.05% NaI in their water develop severe thyroid epithelial cell (thyrocyte) hyperplasia and proliferation (TEC H/P) and fibrosis. Proliferating thyrocytes of IFN-gamma(-/-) mice with TEC H/P produce TGF-beta as demonstrated by immunohistochemical staining and in situ hybridization. Strong expression of activating phosphorylated Smad-2/3 and weak expression of inhibitory Smad-7 by proliferating thyrocytes correlate with the severity of TEC H/P. Splenocytes from IFN-gamma(-/-) mice with severe TEC H/P transfer severe TEC H/P to IFN-gamma(-/-)NOD.H-2h4.SCID mice. Mice given anti-TGF-beta had markedly reduced thyrocyte proliferation and decreased fibrosis compared with mouse Ig-treated controls, suggesting that TGF-beta plays an important role in development of TEC H/P induced by activated splenocytes. Moreover, transgenic IFN-gamma(-/-)NOD.H-2h4 mice expressing TGF-beta on thyrocytes all develop fibrosis and moderate to severe TEC H/P with accelerated kinetics, directly demonstrating a role for TGF-beta in severe TEC H/P and fibrosis.</abstract><cop>United States</cop><pmid>18641364</pmid><doi>10.4049/jimmunol.181.3.2238</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Alma/SFX Local Collection; EZB Electronic Journals Library |
| subjects | Animals Antibodies - immunology Cell Proliferation Epithelial Cells - cytology Epithelial Cells - metabolism Fibrosis - genetics Fibrosis - metabolism Fibrosis - pathology Interferon-gamma - deficiency Interferon-gamma - genetics Interferon-gamma - metabolism Mice Mice, Inbred NOD Mice, Knockout Phosphorylation Protein-Serine-Threonine Kinases - metabolism Receptor, Transforming Growth Factor-beta Type II Receptors, Transforming Growth Factor beta - metabolism Smad2 Protein - metabolism Smad3 Protein - metabolism Spleen - immunology Spleen - metabolism Thymus Hyperplasia - genetics Thymus Hyperplasia - metabolism Thymus Hyperplasia - pathology Transforming Growth Factor beta - genetics Transforming Growth Factor beta - immunology Transforming Growth Factor beta - metabolism |
| title | TGF-beta promotes thyroid epithelial cell hyperplasia and fibrosis in IFN-gamma-deficient NOD.H-2h4 mice |
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