Differential gene expression analysis of iodide-treated rat thyroid follicular cell line PCCl3
The inhibitory effect of supraphysiological iodide concentrations on thyroid hormone synthesis (Wolff–Chaikoff effect) and on thyrocyte proliferation is largely known as iodine autoregulation. However, the molecular mechanisms by which iodide modulates thyroid function remain unclear. In this paper,...
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Veröffentlicht in: | Genomics (San Diego, Calif.) Calif.), 2008-04, Vol.91 (4), p.356-366 |
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creator | Leoni, S.G. Galante, P.A. Ricarte-Filho, J.C.M. Kimura, E.T. |
description | The inhibitory effect of supraphysiological iodide concentrations on thyroid hormone synthesis (Wolff–Chaikoff effect) and on thyrocyte proliferation is largely known as iodine autoregulation. However, the molecular mechanisms by which iodide modulates thyroid function remain unclear. In this paper, we analyze the transcriptome profile of the rat follicular cell lineage PCCl3 under untreated and treated conditions with 10
−
3
M sodium iodide (NaI). Serial analysis of gene expression (SAGE) revealed 84 transcripts differentially expressed in response to iodide (
p
≤
0.001). We also showed that iodide excess inhibits the expression of essential genes for thyroid differentiation:
Tshr,
Nis,
Tg, and
Tpo. Relative expression of 14 of 20 transcripts selected by SAGE was confirmed by real-time PCR. Considering the key role of iodide organification in thyroid physiology, we also observed that both the oxidized form of iodide and iodide per se are responsible for gene expression modulation in response to iodide excess. |
doi_str_mv | 10.1016/j.ygeno.2007.12.009 |
format | Article |
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−
3
M sodium iodide (NaI). Serial analysis of gene expression (SAGE) revealed 84 transcripts differentially expressed in response to iodide (
p
≤
0.001). We also showed that iodide excess inhibits the expression of essential genes for thyroid differentiation:
Tshr,
Nis,
Tg, and
Tpo. Relative expression of 14 of 20 transcripts selected by SAGE was confirmed by real-time PCR. Considering the key role of iodide organification in thyroid physiology, we also observed that both the oxidized form of iodide and iodide per se are responsible for gene expression modulation in response to iodide excess.</description><identifier>ISSN: 0888-7543</identifier><identifier>EISSN: 1089-8646</identifier><identifier>DOI: 10.1016/j.ygeno.2007.12.009</identifier><identifier>PMID: 18272324</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Autoregulation ; Base Sequence ; Cell Line ; Differential gene expression ; Gene Expression Profiling ; Iodides - pharmacology ; Iodine ; Iodine excess ; Methimazole ; PCCl3 lineage ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; SAGE ; Thyroid ; Thyroid differentiation ; Thyroid Gland - cytology ; Thyroid Gland - drug effects ; Thyroid Gland - metabolism ; Transcriptome</subject><ispartof>Genomics (San Diego, Calif.), 2008-04, Vol.91 (4), p.356-366</ispartof><rights>2008 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c454t-545c1a739cb839cd3a01beab6a10a70826f2a1e38a9e8e51953ab3db190bc34b3</citedby><cites>FETCH-LOGICAL-c454t-545c1a739cb839cd3a01beab6a10a70826f2a1e38a9e8e51953ab3db190bc34b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ygeno.2007.12.009$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18272324$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Leoni, S.G.</creatorcontrib><creatorcontrib>Galante, P.A.</creatorcontrib><creatorcontrib>Ricarte-Filho, J.C.M.</creatorcontrib><creatorcontrib>Kimura, E.T.</creatorcontrib><title>Differential gene expression analysis of iodide-treated rat thyroid follicular cell line PCCl3</title><title>Genomics (San Diego, Calif.)</title><addtitle>Genomics</addtitle><description>The inhibitory effect of supraphysiological iodide concentrations on thyroid hormone synthesis (Wolff–Chaikoff effect) and on thyrocyte proliferation is largely known as iodine autoregulation. However, the molecular mechanisms by which iodide modulates thyroid function remain unclear. In this paper, we analyze the transcriptome profile of the rat follicular cell lineage PCCl3 under untreated and treated conditions with 10
−
3
M sodium iodide (NaI). Serial analysis of gene expression (SAGE) revealed 84 transcripts differentially expressed in response to iodide (
p
≤
0.001). We also showed that iodide excess inhibits the expression of essential genes for thyroid differentiation:
Tshr,
Nis,
Tg, and
Tpo. Relative expression of 14 of 20 transcripts selected by SAGE was confirmed by real-time PCR. Considering the key role of iodide organification in thyroid physiology, we also observed that both the oxidized form of iodide and iodide per se are responsible for gene expression modulation in response to iodide excess.</description><subject>Animals</subject><subject>Autoregulation</subject><subject>Base Sequence</subject><subject>Cell Line</subject><subject>Differential gene expression</subject><subject>Gene Expression Profiling</subject><subject>Iodides - pharmacology</subject><subject>Iodine</subject><subject>Iodine excess</subject><subject>Methimazole</subject><subject>PCCl3 lineage</subject><subject>Rats</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>SAGE</subject><subject>Thyroid</subject><subject>Thyroid differentiation</subject><subject>Thyroid Gland - cytology</subject><subject>Thyroid Gland - drug effects</subject><subject>Thyroid Gland - metabolism</subject><subject>Transcriptome</subject><issn>0888-7543</issn><issn>1089-8646</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1vEzEQQC0EomnKL0CqfOK2i7921z70gEJLkSrBgV5rzdqz4MhZp_amIv--GxKpN3rxXN68sR4hHzmrOePt53W9_41jqgVjXc1FzZh5QxacaVPpVrVvyYJprauuUfKMnJeyZjMhtXhPzrgWnZBCLcjD1zAMmHGcAkQ6-5Di323GUkIaKYwQ9yUUmgYakg8eqykjTOhpholOf_Y5BU-HFGNwuwiZOoyRxjBrfq5WUV6QdwPEgh9Oc0nub65_rW6rux_fvq--3FVONWqqGtU4Dp00rtfz4yUw3iP0LXAGHdOiHQRwlBoMamy4aST00vfcsN5J1csl-XT0bnN63GGZ7CaUw19gxLQrtmNKGiObV0FuOtZprWZQHkGXUykZB7vNYQN5bzmzh_52bf_1t4f-lgt7qLsklyf9rt-gf9k5BZ-BqyOAc42ngNkWF3B06ENGN1mfwn8PPANGQJiH</recordid><startdate>20080401</startdate><enddate>20080401</enddate><creator>Leoni, S.G.</creator><creator>Galante, P.A.</creator><creator>Ricarte-Filho, J.C.M.</creator><creator>Kimura, E.T.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><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>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20080401</creationdate><title>Differential gene expression analysis of iodide-treated rat thyroid follicular cell line PCCl3</title><author>Leoni, S.G. ; Galante, P.A. ; Ricarte-Filho, J.C.M. ; Kimura, E.T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-545c1a739cb839cd3a01beab6a10a70826f2a1e38a9e8e51953ab3db190bc34b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Autoregulation</topic><topic>Base Sequence</topic><topic>Cell Line</topic><topic>Differential gene expression</topic><topic>Gene Expression Profiling</topic><topic>Iodides - pharmacology</topic><topic>Iodine</topic><topic>Iodine excess</topic><topic>Methimazole</topic><topic>PCCl3 lineage</topic><topic>Rats</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>SAGE</topic><topic>Thyroid</topic><topic>Thyroid differentiation</topic><topic>Thyroid Gland - cytology</topic><topic>Thyroid Gland - drug effects</topic><topic>Thyroid Gland - metabolism</topic><topic>Transcriptome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Leoni, S.G.</creatorcontrib><creatorcontrib>Galante, P.A.</creatorcontrib><creatorcontrib>Ricarte-Filho, J.C.M.</creatorcontrib><creatorcontrib>Kimura, E.T.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genomics (San Diego, Calif.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Leoni, S.G.</au><au>Galante, P.A.</au><au>Ricarte-Filho, J.C.M.</au><au>Kimura, E.T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential gene expression analysis of iodide-treated rat thyroid follicular cell line PCCl3</atitle><jtitle>Genomics (San Diego, Calif.)</jtitle><addtitle>Genomics</addtitle><date>2008-04-01</date><risdate>2008</risdate><volume>91</volume><issue>4</issue><spage>356</spage><epage>366</epage><pages>356-366</pages><issn>0888-7543</issn><eissn>1089-8646</eissn><abstract>The inhibitory effect of supraphysiological iodide concentrations on thyroid hormone synthesis (Wolff–Chaikoff effect) and on thyrocyte proliferation is largely known as iodine autoregulation. However, the molecular mechanisms by which iodide modulates thyroid function remain unclear. In this paper, we analyze the transcriptome profile of the rat follicular cell lineage PCCl3 under untreated and treated conditions with 10
−
3
M sodium iodide (NaI). Serial analysis of gene expression (SAGE) revealed 84 transcripts differentially expressed in response to iodide (
p
≤
0.001). We also showed that iodide excess inhibits the expression of essential genes for thyroid differentiation:
Tshr,
Nis,
Tg, and
Tpo. Relative expression of 14 of 20 transcripts selected by SAGE was confirmed by real-time PCR. Considering the key role of iodide organification in thyroid physiology, we also observed that both the oxidized form of iodide and iodide per se are responsible for gene expression modulation in response to iodide excess.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>18272324</pmid><doi>10.1016/j.ygeno.2007.12.009</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Autoregulation Base Sequence Cell Line Differential gene expression Gene Expression Profiling Iodides - pharmacology Iodine Iodine excess Methimazole PCCl3 lineage Rats Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics SAGE Thyroid Thyroid differentiation Thyroid Gland - cytology Thyroid Gland - drug effects Thyroid Gland - metabolism Transcriptome |
title | Differential gene expression analysis of iodide-treated rat thyroid follicular cell line PCCl3 |
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