MicroRNA-98 negatively regulates IL-10 production and endotoxin tolerance in macrophages after LPS stimulation
► miR-98 expression is markedly decreased in macrophages following LPS stimulation. ► miR-98 targets the 3’untranslated region of IL-10 transcript. ► Overexpression of miR-98 inhibited TLR4-triggered IL-10 production. ► Furthermore, miR-98 significantly mitigated the induction of endotoxin tolerance...
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| Veröffentlicht in: | FEBS letters 2011-06, Vol.585 (12), p.1963-1968 |
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| container_issue | 12 |
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| container_title | FEBS letters |
| container_volume | 585 |
| creator | Liu, Yang Chen, Qingyun Song, Yinjing Lai, Lihua Wang, Jianli Yu, Hai Cao, Xuetao Wang, Qingqing |
| description | ► miR-98 expression is markedly decreased in macrophages following LPS stimulation. ► miR-98 targets the 3’untranslated region of IL-10 transcript. ► Overexpression of miR-98 inhibited TLR4-triggered IL-10 production. ► Furthermore, miR-98 significantly mitigated the induction of endotoxin tolerance. ► We conclude that miR-98 is involved in fine tuning the level of TLR4-triggered IL-10 production.
Interleukin 10 (IL-10) is a potent anti-inflammatory cytokine that is crucial for dampening the inflammatory response after pathogen invasion, and was found to be produced by macrophages after exposure to lipopolysaccharide (LPS). It remains unclear whether microRNA-mediated regulatory mechanism is involved in LPS-induced IL-10 production. Here we reported that miR-98 expression in macrophages significantly decreased following LPS stimulation. We also found that miR-98 targets the 3’untranslated region of IL-10 transcript. Overexpression of miR-98 inhibited TLR4-triggered IL-10 production and promoted COX-2 expression. We further demonstrated that miR-98 significantly mitigated the induction of endotoxin tolerance, suggesting that miR-98-mediated posttranscriptional control could potentially be involved in fine tuning the critical level of IL-10 production in endotoxin tolerance. |
| doi_str_mv | 10.1016/j.febslet.2011.05.029 |
| format | Article |
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Interleukin 10 (IL-10) is a potent anti-inflammatory cytokine that is crucial for dampening the inflammatory response after pathogen invasion, and was found to be produced by macrophages after exposure to lipopolysaccharide (LPS). It remains unclear whether microRNA-mediated regulatory mechanism is involved in LPS-induced IL-10 production. Here we reported that miR-98 expression in macrophages significantly decreased following LPS stimulation. We also found that miR-98 targets the 3’untranslated region of IL-10 transcript. Overexpression of miR-98 inhibited TLR4-triggered IL-10 production and promoted COX-2 expression. We further demonstrated that miR-98 significantly mitigated the induction of endotoxin tolerance, suggesting that miR-98-mediated posttranscriptional control could potentially be involved in fine tuning the critical level of IL-10 production in endotoxin tolerance.</description><identifier>ISSN: 0014-5793</identifier><identifier>EISSN: 1873-3468</identifier><identifier>DOI: 10.1016/j.febslet.2011.05.029</identifier><identifier>PMID: 21609717</identifier><language>eng</language><publisher>England: Elsevier B.V</publisher><subject>Animals ; COX-2 ; cyclooxygenase-2 ; Drug Tolerance ; Endotoxin tolerance ; Endotoxins - pharmacology ; FBS ; fetal bovine serum ; Gene Expression Regulation ; Humans ; interferon regulatory factor 3 ; interleukin ; Interleukin 10 ; Interleukin-10 - biosynthesis ; Interleukin-10 - genetics ; IRF3 ; lipopolysaccharide ; Lipopolysaccharides - pharmacology ; LPS ; Macrophage ; Macrophages - metabolism ; Mice ; microRNA-98 ; MicroRNAs - physiology ; MyD88 ; myeloid differentiation primary-response protein 88 ; PBMC ; peripheral blood mononuclear cell ; TGF-β ; TIR-domain-containing adapter-inducing interferon β ; TLR ; TNF receptor-associated factor 3 ; TNF-α ; toll-like receptors ; TRAF3 ; transforming growth factor β ; TRIF ; tumor necrosis factor α</subject><ispartof>FEBS letters, 2011-06, Vol.585 (12), p.1963-1968</ispartof><rights>2011 Federation of European Biochemical Societies</rights><rights>FEBS Letters 585 (2011) 1873-3468 © 2015 Federation of European Biochemical Societies</rights><rights>Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5740-3615f2f2ba4b6b19666b51cc7976db9aff8e72a18b3c67227e5160028dec50263</citedby><cites>FETCH-LOGICAL-c5740-3615f2f2ba4b6b19666b51cc7976db9aff8e72a18b3c67227e5160028dec50263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1016%2Fj.febslet.2011.05.029$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014579311003930$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,1411,1427,3537,27901,27902,45550,45551,46384,46808,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21609717$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Yang</creatorcontrib><creatorcontrib>Chen, Qingyun</creatorcontrib><creatorcontrib>Song, Yinjing</creatorcontrib><creatorcontrib>Lai, Lihua</creatorcontrib><creatorcontrib>Wang, Jianli</creatorcontrib><creatorcontrib>Yu, Hai</creatorcontrib><creatorcontrib>Cao, Xuetao</creatorcontrib><creatorcontrib>Wang, Qingqing</creatorcontrib><title>MicroRNA-98 negatively regulates IL-10 production and endotoxin tolerance in macrophages after LPS stimulation</title><title>FEBS letters</title><addtitle>FEBS Lett</addtitle><description>► miR-98 expression is markedly decreased in macrophages following LPS stimulation. ► miR-98 targets the 3’untranslated region of IL-10 transcript. ► Overexpression of miR-98 inhibited TLR4-triggered IL-10 production. ► Furthermore, miR-98 significantly mitigated the induction of endotoxin tolerance. ► We conclude that miR-98 is involved in fine tuning the level of TLR4-triggered IL-10 production.
Interleukin 10 (IL-10) is a potent anti-inflammatory cytokine that is crucial for dampening the inflammatory response after pathogen invasion, and was found to be produced by macrophages after exposure to lipopolysaccharide (LPS). It remains unclear whether microRNA-mediated regulatory mechanism is involved in LPS-induced IL-10 production. Here we reported that miR-98 expression in macrophages significantly decreased following LPS stimulation. We also found that miR-98 targets the 3’untranslated region of IL-10 transcript. Overexpression of miR-98 inhibited TLR4-triggered IL-10 production and promoted COX-2 expression. We further demonstrated that miR-98 significantly mitigated the induction of endotoxin tolerance, suggesting that miR-98-mediated posttranscriptional control could potentially be involved in fine tuning the critical level of IL-10 production in endotoxin tolerance.</description><subject>Animals</subject><subject>COX-2</subject><subject>cyclooxygenase-2</subject><subject>Drug Tolerance</subject><subject>Endotoxin tolerance</subject><subject>Endotoxins - pharmacology</subject><subject>FBS</subject><subject>fetal bovine serum</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>interferon regulatory factor 3</subject><subject>interleukin</subject><subject>Interleukin 10</subject><subject>Interleukin-10 - biosynthesis</subject><subject>Interleukin-10 - genetics</subject><subject>IRF3</subject><subject>lipopolysaccharide</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>LPS</subject><subject>Macrophage</subject><subject>Macrophages - metabolism</subject><subject>Mice</subject><subject>microRNA-98</subject><subject>MicroRNAs - physiology</subject><subject>MyD88</subject><subject>myeloid differentiation primary-response protein 88</subject><subject>PBMC</subject><subject>peripheral blood mononuclear cell</subject><subject>TGF-β</subject><subject>TIR-domain-containing adapter-inducing interferon β</subject><subject>TLR</subject><subject>TNF receptor-associated factor 3</subject><subject>TNF-α</subject><subject>toll-like receptors</subject><subject>TRAF3</subject><subject>transforming growth factor β</subject><subject>TRIF</subject><subject>tumor necrosis factor α</subject><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU9v1DAQxS0EokvhI4B845QwtmM7PqFStbTS8kcUzpbjTBavsskSOy377XG0C9dyskZ67_nN_Ah5zaBkwNS7bdlhE3tMJQfGSpAlcPOErFitRSEqVT8lKwBWFVIbcUZexLiFPNfMPCdnnCkwmukVGT4FP43fPl8UpqYDblwK99gf6ISbuXcJI71dFwzofhrb2acwDtQNLcWhHdP4Oww0jT1ObvBI87BzOWz_022yz3UJJ7r-ekdjCrslLJtfkmed6yO-Or3n5Mf11ffLm2L95ePt5cW68FJXUAjFZMc73riqUQ0zSqlGMu-10aptjOu6GjV3rG6EV5pzjTJvBLxu0UvgSpyTt8fc3PvXjDHZXYge-94NOM7RGqgqLUHKR5W1ZqJmooKslEdl3jHGCTu7n8LOTQfLwC5M7NaemNiFiQVpM5Pse3P6YW522P5z_YWQBTdHwUPo8fB_qfb66gO_WwAvfBkDEEYsHd8fozAf9z7gZKMPmOm0YUKfbDuGR9r-AaxxtOs</recordid><startdate>20110623</startdate><enddate>20110623</enddate><creator>Liu, Yang</creator><creator>Chen, Qingyun</creator><creator>Song, Yinjing</creator><creator>Lai, Lihua</creator><creator>Wang, Jianli</creator><creator>Yu, Hai</creator><creator>Cao, Xuetao</creator><creator>Wang, Qingqing</creator><general>Elsevier B.V</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>7X8</scope><scope>7T7</scope><scope>7TM</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>20110623</creationdate><title>MicroRNA-98 negatively regulates IL-10 production and endotoxin tolerance in macrophages after LPS stimulation</title><author>Liu, Yang ; Chen, Qingyun ; Song, Yinjing ; Lai, Lihua ; Wang, Jianli ; Yu, Hai ; Cao, Xuetao ; Wang, Qingqing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5740-3615f2f2ba4b6b19666b51cc7976db9aff8e72a18b3c67227e5160028dec50263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>COX-2</topic><topic>cyclooxygenase-2</topic><topic>Drug Tolerance</topic><topic>Endotoxin tolerance</topic><topic>Endotoxins - pharmacology</topic><topic>FBS</topic><topic>fetal bovine serum</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>interferon regulatory factor 3</topic><topic>interleukin</topic><topic>Interleukin 10</topic><topic>Interleukin-10 - biosynthesis</topic><topic>Interleukin-10 - genetics</topic><topic>IRF3</topic><topic>lipopolysaccharide</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>LPS</topic><topic>Macrophage</topic><topic>Macrophages - metabolism</topic><topic>Mice</topic><topic>microRNA-98</topic><topic>MicroRNAs - physiology</topic><topic>MyD88</topic><topic>myeloid differentiation primary-response protein 88</topic><topic>PBMC</topic><topic>peripheral blood mononuclear cell</topic><topic>TGF-β</topic><topic>TIR-domain-containing adapter-inducing interferon β</topic><topic>TLR</topic><topic>TNF receptor-associated factor 3</topic><topic>TNF-α</topic><topic>toll-like receptors</topic><topic>TRAF3</topic><topic>transforming growth factor β</topic><topic>TRIF</topic><topic>tumor necrosis factor α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Yang</creatorcontrib><creatorcontrib>Chen, Qingyun</creatorcontrib><creatorcontrib>Song, Yinjing</creatorcontrib><creatorcontrib>Lai, Lihua</creatorcontrib><creatorcontrib>Wang, Jianli</creatorcontrib><creatorcontrib>Yu, Hai</creatorcontrib><creatorcontrib>Cao, Xuetao</creatorcontrib><creatorcontrib>Wang, Qingqing</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>MEDLINE - Academic</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Yang</au><au>Chen, Qingyun</au><au>Song, Yinjing</au><au>Lai, Lihua</au><au>Wang, Jianli</au><au>Yu, Hai</au><au>Cao, Xuetao</au><au>Wang, Qingqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-98 negatively regulates IL-10 production and endotoxin tolerance in macrophages after LPS stimulation</atitle><jtitle>FEBS letters</jtitle><addtitle>FEBS Lett</addtitle><date>2011-06-23</date><risdate>2011</risdate><volume>585</volume><issue>12</issue><spage>1963</spage><epage>1968</epage><pages>1963-1968</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><abstract>► miR-98 expression is markedly decreased in macrophages following LPS stimulation. ► miR-98 targets the 3’untranslated region of IL-10 transcript. ► Overexpression of miR-98 inhibited TLR4-triggered IL-10 production. ► Furthermore, miR-98 significantly mitigated the induction of endotoxin tolerance. ► We conclude that miR-98 is involved in fine tuning the level of TLR4-triggered IL-10 production.
Interleukin 10 (IL-10) is a potent anti-inflammatory cytokine that is crucial for dampening the inflammatory response after pathogen invasion, and was found to be produced by macrophages after exposure to lipopolysaccharide (LPS). It remains unclear whether microRNA-mediated regulatory mechanism is involved in LPS-induced IL-10 production. Here we reported that miR-98 expression in macrophages significantly decreased following LPS stimulation. We also found that miR-98 targets the 3’untranslated region of IL-10 transcript. Overexpression of miR-98 inhibited TLR4-triggered IL-10 production and promoted COX-2 expression. We further demonstrated that miR-98 significantly mitigated the induction of endotoxin tolerance, suggesting that miR-98-mediated posttranscriptional control could potentially be involved in fine tuning the critical level of IL-10 production in endotoxin tolerance.</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>21609717</pmid><doi>10.1016/j.febslet.2011.05.029</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | FEBS letters, 2011-06, Vol.585 (12), p.1963-1968 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Elsevier ScienceDirect Journals; Wiley Online Library Free Content; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals COX-2 cyclooxygenase-2 Drug Tolerance Endotoxin tolerance Endotoxins - pharmacology FBS fetal bovine serum Gene Expression Regulation Humans interferon regulatory factor 3 interleukin Interleukin 10 Interleukin-10 - biosynthesis Interleukin-10 - genetics IRF3 lipopolysaccharide Lipopolysaccharides - pharmacology LPS Macrophage Macrophages - metabolism Mice microRNA-98 MicroRNAs - physiology MyD88 myeloid differentiation primary-response protein 88 PBMC peripheral blood mononuclear cell TGF-β TIR-domain-containing adapter-inducing interferon β TLR TNF receptor-associated factor 3 TNF-α toll-like receptors TRAF3 transforming growth factor β TRIF tumor necrosis factor α |
| title | MicroRNA-98 negatively regulates IL-10 production and endotoxin tolerance in macrophages after LPS stimulation |
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