Resveratrol post-transcriptionally regulates pro-inflammatory gene expression via regulation of KSRP RNA binding activity
Resveratrol shows beneficial effects in inflammation-based diseases like cancer, cardiovascular and chronic inflammatory diseases. Therefore, the molecular mechanisms of the anti-inflammatory resveratrol effects deserve more attention. In human epithelial DLD-1 and monocytic Mono Mac 6 cells resvera...
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| Veröffentlicht in: | Nucleic acids research 2014-11, Vol.42 (20), p.12555-12569 |
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| creator | Bollmann, Franziska Art, Julia Henke, Jenny Schrick, Katharina Besche, Verena Bros, Matthias Li, Huige Siuda, Daniel Handler, Norbert Bauer, Florian Erker, Thomas Behnke, Felix Mönch, Bettina Härdle, Lorena Hoffmann, Markus Chen, Ching-Yi Förstermann, Ulrich Dirsch, Verena M Werz, Oliver Kleinert, Hartmut Pautz, Andrea |
| description | Resveratrol shows beneficial effects in inflammation-based diseases like cancer, cardiovascular and chronic inflammatory diseases. Therefore, the molecular mechanisms of the anti-inflammatory resveratrol effects deserve more attention. In human epithelial DLD-1 and monocytic Mono Mac 6 cells resveratrol decreased the expression of iNOS, IL-8 and TNF-α by reducing mRNA stability without inhibition of the promoter activity. Shown by pharmacological and siRNA-mediated inhibition, the observed effects are SIRT1-independent. Target-fishing and drug responsive target stability experiments showed selective binding of resveratrol to the RNA-binding protein KSRP, a central post-transcriptional regulator of pro-inflammatory gene expression. Knockdown of KSRP expression prevented resveratrol-induced mRNA destabilization in human and murine cells. Resveratrol did not change KSRP expression, but immunoprecipitation experiments indicated that resveratrol reduces the p38 MAPK-related inhibitory KSRP threonine phosphorylation, without blocking p38 MAPK activation or activity. Mutation of the p38 MAPK target site in KSRP blocked the resveratrol effect on pro-inflammatory gene expression. In addition, resveratrol incubation enhanced KSRP-exosome interaction, which is important for mRNA degradation. Finally, resveratrol incubation enhanced its intra-cellular binding to the IL-8, iNOS and TNF-α mRNA. Therefore, modulation of KSRP mRNA binding activity and, thereby, enhancement of mRNA degradation seems to be the common denominator of many anti-inflammatory effects of resveratrol. |
| doi_str_mv | 10.1093/nar/gku1033 |
| format | Article |
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Therefore, the molecular mechanisms of the anti-inflammatory resveratrol effects deserve more attention. In human epithelial DLD-1 and monocytic Mono Mac 6 cells resveratrol decreased the expression of iNOS, IL-8 and TNF-α by reducing mRNA stability without inhibition of the promoter activity. Shown by pharmacological and siRNA-mediated inhibition, the observed effects are SIRT1-independent. Target-fishing and drug responsive target stability experiments showed selective binding of resveratrol to the RNA-binding protein KSRP, a central post-transcriptional regulator of pro-inflammatory gene expression. Knockdown of KSRP expression prevented resveratrol-induced mRNA destabilization in human and murine cells. Resveratrol did not change KSRP expression, but immunoprecipitation experiments indicated that resveratrol reduces the p38 MAPK-related inhibitory KSRP threonine phosphorylation, without blocking p38 MAPK activation or activity. Mutation of the p38 MAPK target site in KSRP blocked the resveratrol effect on pro-inflammatory gene expression. In addition, resveratrol incubation enhanced KSRP-exosome interaction, which is important for mRNA degradation. Finally, resveratrol incubation enhanced its intra-cellular binding to the IL-8, iNOS and TNF-α mRNA. Therefore, modulation of KSRP mRNA binding activity and, thereby, enhancement of mRNA degradation seems to be the common denominator of many anti-inflammatory effects of resveratrol.</description><identifier>ISSN: 0305-1048</identifier><identifier>EISSN: 1362-4962</identifier><identifier>DOI: 10.1093/nar/gku1033</identifier><identifier>PMID: 25352548</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Animals ; Anti-Inflammatory Agents, Non-Steroidal - pharmacology ; Cell Line, Tumor ; Exosome Multienzyme Ribonuclease Complex - metabolism ; Gene Expression - drug effects ; Gene regulation, Chromatin and Epigenetics ; Humans ; Inflammation Mediators - metabolism ; Mice ; Mice, Knockout ; Mutation ; p38 Mitogen-Activated Protein Kinases - metabolism ; Resveratrol ; RNA Stability - drug effects ; RNA, Messenger - metabolism ; RNA-Binding Proteins - genetics ; RNA-Binding Proteins - metabolism ; Stilbenes - pharmacology ; Trans-Activators - genetics ; Trans-Activators - metabolism</subject><ispartof>Nucleic acids research, 2014-11, Vol.42 (20), p.12555-12569</ispartof><rights>The Author(s) 2014. Published by Oxford University Press on behalf of Nucleic Acids Research.</rights><rights>The Author(s) 2014. Published by Oxford University Press on behalf of Nucleic Acids Research. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c480t-e898d7ebc23e368fe14cf1d4532827c42297cd7a072430e67a35053a5d957bde3</citedby><cites>FETCH-LOGICAL-c480t-e898d7ebc23e368fe14cf1d4532827c42297cd7a072430e67a35053a5d957bde3</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/PMC4227754/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4227754/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25352548$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bollmann, Franziska</creatorcontrib><creatorcontrib>Art, Julia</creatorcontrib><creatorcontrib>Henke, Jenny</creatorcontrib><creatorcontrib>Schrick, Katharina</creatorcontrib><creatorcontrib>Besche, Verena</creatorcontrib><creatorcontrib>Bros, Matthias</creatorcontrib><creatorcontrib>Li, Huige</creatorcontrib><creatorcontrib>Siuda, Daniel</creatorcontrib><creatorcontrib>Handler, Norbert</creatorcontrib><creatorcontrib>Bauer, Florian</creatorcontrib><creatorcontrib>Erker, Thomas</creatorcontrib><creatorcontrib>Behnke, Felix</creatorcontrib><creatorcontrib>Mönch, Bettina</creatorcontrib><creatorcontrib>Härdle, Lorena</creatorcontrib><creatorcontrib>Hoffmann, Markus</creatorcontrib><creatorcontrib>Chen, Ching-Yi</creatorcontrib><creatorcontrib>Förstermann, Ulrich</creatorcontrib><creatorcontrib>Dirsch, Verena M</creatorcontrib><creatorcontrib>Werz, Oliver</creatorcontrib><creatorcontrib>Kleinert, Hartmut</creatorcontrib><creatorcontrib>Pautz, Andrea</creatorcontrib><title>Resveratrol post-transcriptionally regulates pro-inflammatory gene expression via regulation of KSRP RNA binding activity</title><title>Nucleic acids research</title><addtitle>Nucleic Acids Res</addtitle><description>Resveratrol shows beneficial effects in inflammation-based diseases like cancer, cardiovascular and chronic inflammatory diseases. Therefore, the molecular mechanisms of the anti-inflammatory resveratrol effects deserve more attention. In human epithelial DLD-1 and monocytic Mono Mac 6 cells resveratrol decreased the expression of iNOS, IL-8 and TNF-α by reducing mRNA stability without inhibition of the promoter activity. Shown by pharmacological and siRNA-mediated inhibition, the observed effects are SIRT1-independent. Target-fishing and drug responsive target stability experiments showed selective binding of resveratrol to the RNA-binding protein KSRP, a central post-transcriptional regulator of pro-inflammatory gene expression. Knockdown of KSRP expression prevented resveratrol-induced mRNA destabilization in human and murine cells. Resveratrol did not change KSRP expression, but immunoprecipitation experiments indicated that resveratrol reduces the p38 MAPK-related inhibitory KSRP threonine phosphorylation, without blocking p38 MAPK activation or activity. Mutation of the p38 MAPK target site in KSRP blocked the resveratrol effect on pro-inflammatory gene expression. In addition, resveratrol incubation enhanced KSRP-exosome interaction, which is important for mRNA degradation. Finally, resveratrol incubation enhanced its intra-cellular binding to the IL-8, iNOS and TNF-α mRNA. 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Therefore, the molecular mechanisms of the anti-inflammatory resveratrol effects deserve more attention. In human epithelial DLD-1 and monocytic Mono Mac 6 cells resveratrol decreased the expression of iNOS, IL-8 and TNF-α by reducing mRNA stability without inhibition of the promoter activity. Shown by pharmacological and siRNA-mediated inhibition, the observed effects are SIRT1-independent. Target-fishing and drug responsive target stability experiments showed selective binding of resveratrol to the RNA-binding protein KSRP, a central post-transcriptional regulator of pro-inflammatory gene expression. Knockdown of KSRP expression prevented resveratrol-induced mRNA destabilization in human and murine cells. Resveratrol did not change KSRP expression, but immunoprecipitation experiments indicated that resveratrol reduces the p38 MAPK-related inhibitory KSRP threonine phosphorylation, without blocking p38 MAPK activation or activity. Mutation of the p38 MAPK target site in KSRP blocked the resveratrol effect on pro-inflammatory gene expression. In addition, resveratrol incubation enhanced KSRP-exosome interaction, which is important for mRNA degradation. Finally, resveratrol incubation enhanced its intra-cellular binding to the IL-8, iNOS and TNF-α mRNA. Therefore, modulation of KSRP mRNA binding activity and, thereby, enhancement of mRNA degradation seems to be the common denominator of many anti-inflammatory effects of resveratrol.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>25352548</pmid><doi>10.1093/nar/gku1033</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anti-Inflammatory Agents, Non-Steroidal - pharmacology Cell Line, Tumor Exosome Multienzyme Ribonuclease Complex - metabolism Gene Expression - drug effects Gene regulation, Chromatin and Epigenetics Humans Inflammation Mediators - metabolism Mice Mice, Knockout Mutation p38 Mitogen-Activated Protein Kinases - metabolism Resveratrol RNA Stability - drug effects RNA, Messenger - metabolism RNA-Binding Proteins - genetics RNA-Binding Proteins - metabolism Stilbenes - pharmacology Trans-Activators - genetics Trans-Activators - metabolism |
| title | Resveratrol post-transcriptionally regulates pro-inflammatory gene expression via regulation of KSRP RNA binding activity |
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