MCPIP1 down-regulates IL-2 expression through an ARE-independent pathway
IL-2 plays a key role in the survival and proliferation of immune cells, especially T lymphocytes. Its expression is precisely regulated at transcriptional and posttranscriptional level. IL-2 is known to be regulated by RNA binding proteins, such as tristetraprolin (TTP), via an AU-rich element (ARE...
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| Veröffentlicht in: | PloS one 2012-11, Vol.7 (11), p.e49841-e49841 |
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| creator | Li, Min Cao, Wenqiang Liu, Haifeng Zhang, Wei Liu, Xia Cai, Zhijian Guo, Jing Wang, Xuelian Hui, Zhaoyuan Zhang, Hang Wang, Jianli Wang, Lie |
| description | IL-2 plays a key role in the survival and proliferation of immune cells, especially T lymphocytes. Its expression is precisely regulated at transcriptional and posttranscriptional level. IL-2 is known to be regulated by RNA binding proteins, such as tristetraprolin (TTP), via an AU-rich element (ARE) in the 3'-untranslated region (3'UTR) to influence the stability of mRNA. MCPIP1, identified as a novel RNase, can degrade IL-6, IL-12 and TNF-α mRNA by an ARE-independent pathway in the activation of macrophages. Here, we reported that MCPIP1 was induced in the activation of T lymphocytes and negatively regulated IL-2 gene expression in both mouse and human primary T lymphocytes through destabilizing its mRNA. A set of Luciferase reporter assay demonstrated that a non-ARE conserved element in IL-2 3'UTR, which formed a stem-loop structure, responded to MCPIP1 activity.RNA immunoprecipitation and Biotin pulldown experiments further suggested that MCPIP1 could modestly bind to IL-2 mRNA. Taken together, these data demonstrate that MCPIP1 down-regulates IL-2 via an ARE-independent pathway. |
| doi_str_mv | 10.1371/journal.pone.0049841 |
| format | Article |
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Its expression is precisely regulated at transcriptional and posttranscriptional level. IL-2 is known to be regulated by RNA binding proteins, such as tristetraprolin (TTP), via an AU-rich element (ARE) in the 3'-untranslated region (3'UTR) to influence the stability of mRNA. MCPIP1, identified as a novel RNase, can degrade IL-6, IL-12 and TNF-α mRNA by an ARE-independent pathway in the activation of macrophages. Here, we reported that MCPIP1 was induced in the activation of T lymphocytes and negatively regulated IL-2 gene expression in both mouse and human primary T lymphocytes through destabilizing its mRNA. A set of Luciferase reporter assay demonstrated that a non-ARE conserved element in IL-2 3'UTR, which formed a stem-loop structure, responded to MCPIP1 activity.RNA immunoprecipitation and Biotin pulldown experiments further suggested that MCPIP1 could modestly bind to IL-2 mRNA. Taken together, these data demonstrate that MCPIP1 down-regulates IL-2 via an ARE-independent pathway.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0049841</identifier><identifier>PMID: 23185455</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>3' Untranslated regions ; 3' Untranslated Regions - genetics ; Animals ; AU Rich Elements - genetics ; Binding proteins ; Biology ; Biosynthesis ; Biotin ; Cell activation ; Cell Line ; Cell proliferation ; Cell survival ; Cellular biology ; Cytokines ; Ethics ; Gene expression ; Gene Expression Regulation ; Genes ; Humans ; Immune system ; Immunology ; Immunoprecipitation ; Interleukin 12 ; Interleukin 2 ; Interleukin 6 ; Interleukin-12 - metabolism ; Interleukin-2 - genetics ; Interleukin-2 - metabolism ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Kinases ; Luciferase ; Lymphocytes ; Lymphocytes T ; Macrophages ; Medicine ; Messenger RNA ; Mice ; MicroRNAs ; mRNA stability ; Post-transcription ; Protein binding ; Proteins ; Ribonucleases ; Ribonucleic acid ; RNA ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; RNA-binding protein ; RNA-Binding Proteins - genetics ; Rodents ; T cell receptors ; T cells ; T-Lymphocytes - metabolism ; Transcription (Genetics) ; Transcription factors ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Tristetraprolin - metabolism ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2012-11, Vol.7 (11), p.e49841-e49841</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Li et al 2012 Li et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-607f99ced972a8e00aaad28f14cb13dd3f0cb87f9ea1c31b209f413536f2353b3</citedby><cites>FETCH-LOGICAL-c758t-607f99ced972a8e00aaad28f14cb13dd3f0cb87f9ea1c31b209f413536f2353b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504106/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504106/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23185455$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Stoecklin, Georg</contributor><creatorcontrib>Li, Min</creatorcontrib><creatorcontrib>Cao, Wenqiang</creatorcontrib><creatorcontrib>Liu, Haifeng</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><creatorcontrib>Liu, Xia</creatorcontrib><creatorcontrib>Cai, Zhijian</creatorcontrib><creatorcontrib>Guo, Jing</creatorcontrib><creatorcontrib>Wang, Xuelian</creatorcontrib><creatorcontrib>Hui, Zhaoyuan</creatorcontrib><creatorcontrib>Zhang, Hang</creatorcontrib><creatorcontrib>Wang, Jianli</creatorcontrib><creatorcontrib>Wang, Lie</creatorcontrib><title>MCPIP1 down-regulates IL-2 expression through an ARE-independent pathway</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>IL-2 plays a key role in the survival and proliferation of immune cells, especially T lymphocytes. Its expression is precisely regulated at transcriptional and posttranscriptional level. IL-2 is known to be regulated by RNA binding proteins, such as tristetraprolin (TTP), via an AU-rich element (ARE) in the 3'-untranslated region (3'UTR) to influence the stability of mRNA. MCPIP1, identified as a novel RNase, can degrade IL-6, IL-12 and TNF-α mRNA by an ARE-independent pathway in the activation of macrophages. Here, we reported that MCPIP1 was induced in the activation of T lymphocytes and negatively regulated IL-2 gene expression in both mouse and human primary T lymphocytes through destabilizing its mRNA. A set of Luciferase reporter assay demonstrated that a non-ARE conserved element in IL-2 3'UTR, which formed a stem-loop structure, responded to MCPIP1 activity.RNA immunoprecipitation and Biotin pulldown experiments further suggested that MCPIP1 could modestly bind to IL-2 mRNA. Taken together, these data demonstrate that MCPIP1 down-regulates IL-2 via an ARE-independent pathway.</description><subject>3' Untranslated regions</subject><subject>3' Untranslated Regions - genetics</subject><subject>Animals</subject><subject>AU Rich Elements - genetics</subject><subject>Binding proteins</subject><subject>Biology</subject><subject>Biosynthesis</subject><subject>Biotin</subject><subject>Cell activation</subject><subject>Cell Line</subject><subject>Cell proliferation</subject><subject>Cell survival</subject><subject>Cellular biology</subject><subject>Cytokines</subject><subject>Ethics</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Genes</subject><subject>Humans</subject><subject>Immune system</subject><subject>Immunology</subject><subject>Immunoprecipitation</subject><subject>Interleukin 12</subject><subject>Interleukin 2</subject><subject>Interleukin 6</subject><subject>Interleukin-12 - metabolism</subject><subject>Interleukin-2 - genetics</subject><subject>Interleukin-2 - metabolism</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Kinases</subject><subject>Luciferase</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Medicine</subject><subject>Messenger RNA</subject><subject>Mice</subject><subject>MicroRNAs</subject><subject>mRNA stability</subject><subject>Post-transcription</subject><subject>Protein binding</subject><subject>Proteins</subject><subject>Ribonucleases</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA-binding protein</subject><subject>RNA-Binding Proteins - genetics</subject><subject>Rodents</subject><subject>T cell receptors</subject><subject>T cells</subject><subject>T-Lymphocytes - metabolism</subject><subject>Transcription (Genetics)</subject><subject>Transcription factors</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Tristetraprolin - metabolism</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkktr3DAUhU1padK0_6C0hkJpF57qbWlTGIa0GZiSkD62QpblR_BYjiQ3yb-vpuOEccmiGGQhf-fo3uuTJK8hWECcw09XdnS96haD7c0CACI4gU-SYygwyhgC-OnB_ih54f0VABRzxp4nRwhDTgmlx8nZt9XF-gKmpb3pM2fqsVPB-HS9yVBqbgdnvG9tn4bG2bFuUtWny8vTrO1LM5i49CEdVGhu1N3L5FmlOm9eTe-T5OeX0x-rs2xz_nW9Wm4ynVMeMgbySghtSpEjxQ0ASqkS8QoSXUBclrgCuuCRMQpqDAsEREUgpphVKK4FPkne7n2Hzno5DcFLiBHLCceURWK9J0qrruTg2q1yd9KqVv49sK6WyoVWd0aKijNdRKHRmsSaBGY8J1pXOUFMUBq9Pk-3jcXWlDo27FQ3M51_6dtG1va3xBQQCHbFfJgMnL0ejQ9y23ptuk71xo6xboQAZYIREdF3_6CPdzdRtYoNtH1l4716ZyqXJM8BRQTzSC0eoeJTmm2rY2KqNp7PBB9ngsgEcxtqNXov198v_589_zVn3x-wjVFdaLztxhBT5ecg2YPaWe-dqR6GDIHcBf5-GnIXeDkFPsreHP6gB9F9wvEfuf35Fw</recordid><startdate>20121121</startdate><enddate>20121121</enddate><creator>Li, Min</creator><creator>Cao, Wenqiang</creator><creator>Liu, Haifeng</creator><creator>Zhang, Wei</creator><creator>Liu, Xia</creator><creator>Cai, Zhijian</creator><creator>Guo, Jing</creator><creator>Wang, Xuelian</creator><creator>Hui, Zhaoyuan</creator><creator>Zhang, Hang</creator><creator>Wang, Jianli</creator><creator>Wang, Lie</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20121121</creationdate><title>MCPIP1 down-regulates IL-2 expression through an ARE-independent pathway</title><author>Li, Min ; Cao, Wenqiang ; Liu, Haifeng ; Zhang, Wei ; Liu, Xia ; Cai, Zhijian ; Guo, Jing ; Wang, Xuelian ; Hui, Zhaoyuan ; Zhang, Hang ; Wang, Jianli ; Wang, Lie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-607f99ced972a8e00aaad28f14cb13dd3f0cb87f9ea1c31b209f413536f2353b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>3' Untranslated regions</topic><topic>3' Untranslated Regions - genetics</topic><topic>Animals</topic><topic>AU Rich Elements - genetics</topic><topic>Binding proteins</topic><topic>Biology</topic><topic>Biosynthesis</topic><topic>Biotin</topic><topic>Cell activation</topic><topic>Cell Line</topic><topic>Cell proliferation</topic><topic>Cell survival</topic><topic>Cellular biology</topic><topic>Cytokines</topic><topic>Ethics</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Genes</topic><topic>Humans</topic><topic>Immune system</topic><topic>Immunology</topic><topic>Immunoprecipitation</topic><topic>Interleukin 12</topic><topic>Interleukin 2</topic><topic>Interleukin 6</topic><topic>Interleukin-12 - metabolism</topic><topic>Interleukin-2 - genetics</topic><topic>Interleukin-2 - metabolism</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-6 - metabolism</topic><topic>Kinases</topic><topic>Luciferase</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Macrophages</topic><topic>Medicine</topic><topic>Messenger RNA</topic><topic>Mice</topic><topic>MicroRNAs</topic><topic>mRNA stability</topic><topic>Post-transcription</topic><topic>Protein binding</topic><topic>Proteins</topic><topic>Ribonucleases</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Messenger - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Min</au><au>Cao, Wenqiang</au><au>Liu, Haifeng</au><au>Zhang, Wei</au><au>Liu, Xia</au><au>Cai, Zhijian</au><au>Guo, Jing</au><au>Wang, Xuelian</au><au>Hui, Zhaoyuan</au><au>Zhang, Hang</au><au>Wang, Jianli</au><au>Wang, Lie</au><au>Stoecklin, Georg</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MCPIP1 down-regulates IL-2 expression through an ARE-independent pathway</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-11-21</date><risdate>2012</risdate><volume>7</volume><issue>11</issue><spage>e49841</spage><epage>e49841</epage><pages>e49841-e49841</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>IL-2 plays a key role in the survival and proliferation of immune cells, especially T lymphocytes. Its expression is precisely regulated at transcriptional and posttranscriptional level. IL-2 is known to be regulated by RNA binding proteins, such as tristetraprolin (TTP), via an AU-rich element (ARE) in the 3'-untranslated region (3'UTR) to influence the stability of mRNA. MCPIP1, identified as a novel RNase, can degrade IL-6, IL-12 and TNF-α mRNA by an ARE-independent pathway in the activation of macrophages. Here, we reported that MCPIP1 was induced in the activation of T lymphocytes and negatively regulated IL-2 gene expression in both mouse and human primary T lymphocytes through destabilizing its mRNA. A set of Luciferase reporter assay demonstrated that a non-ARE conserved element in IL-2 3'UTR, which formed a stem-loop structure, responded to MCPIP1 activity.RNA immunoprecipitation and Biotin pulldown experiments further suggested that MCPIP1 could modestly bind to IL-2 mRNA. Taken together, these data demonstrate that MCPIP1 down-regulates IL-2 via an ARE-independent pathway.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23185455</pmid><doi>10.1371/journal.pone.0049841</doi><tpages>e49841</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2012-11, Vol.7 (11), p.e49841-e49841 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1326748356 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 3' Untranslated regions 3' Untranslated Regions - genetics Animals AU Rich Elements - genetics Binding proteins Biology Biosynthesis Biotin Cell activation Cell Line Cell proliferation Cell survival Cellular biology Cytokines Ethics Gene expression Gene Expression Regulation Genes Humans Immune system Immunology Immunoprecipitation Interleukin 12 Interleukin 2 Interleukin 6 Interleukin-12 - metabolism Interleukin-2 - genetics Interleukin-2 - metabolism Interleukin-6 - genetics Interleukin-6 - metabolism Kinases Luciferase Lymphocytes Lymphocytes T Macrophages Medicine Messenger RNA Mice MicroRNAs mRNA stability Post-transcription Protein binding Proteins Ribonucleases Ribonucleic acid RNA RNA, Messenger - genetics RNA, Messenger - metabolism RNA-binding protein RNA-Binding Proteins - genetics Rodents T cell receptors T cells T-Lymphocytes - metabolism Transcription (Genetics) Transcription factors Transcription Factors - genetics Transcription Factors - metabolism Tristetraprolin - metabolism Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | MCPIP1 down-regulates IL-2 expression through an ARE-independent pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-30T05%3A57%3A22IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=MCPIP1%20down-regulates%20IL-2%20expression%20through%20an%20ARE-independent%20pathway&rft.jtitle=PloS%20one&rft.au=Li,%20Min&rft.date=2012-11-21&rft.volume=7&rft.issue=11&rft.spage=e49841&rft.epage=e49841&rft.pages=e49841-e49841&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0049841&rft_dat=%3Cgale_plos_%3EA477052438%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1326748356&rft_id=info:pmid/23185455&rft_galeid=A477052438&rft_doaj_id=oai_doaj_org_article_9f86cb674ecc4ed9936874ccf7426955&rfr_iscdi=true |