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RORα is crucial for attenuated inflammatory response to maintain intestinal homeostasisoa mark
  • Oh, Se Kyu ;
  • Kim, Dongha ;
  • Kim, Kyeongkyu ;
  • Boo, Kyungjin ;
  • Yu, Young Suk ;
  • Kim, Ik Soo ;
  • Jeon, Yoon ;
  • Im, Sun Kyoung ;
  • Lee, Su Hyung ;
  • Lee, Ji Min ;
  • Ko, Younhee ;
  • Lee, Ho ;
  • Park, Daechan ;
  • Fang, Sungsoon ;
  • Baek, Sung Hee
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dc.contributor.authorOh, Se Kyu-
dc.contributor.authorKim, Dongha-
dc.contributor.authorKim, Kyeongkyu-
dc.contributor.authorBoo, Kyungjin-
dc.contributor.authorYu, Young Suk-
dc.contributor.authorKim, Ik Soo-
dc.contributor.authorJeon, Yoon-
dc.contributor.authorIm, Sun Kyoung-
dc.contributor.authorLee, Su Hyung-
dc.contributor.authorLee, Ji Min-
dc.contributor.authorKo, Younhee-
dc.contributor.authorLee, Ho-
dc.contributor.authorPark, Daechan-
dc.contributor.authorFang, Sungsoon-
dc.contributor.authorBaek, Sung Hee-
dc.date.issued2019-10-15-
dc.identifier.issn1091-6490-
dc.identifier.urihttps://aurora.ajou.ac.kr/handle/2018.oak/30962-
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85073308098&origin=inward-
dc.description.abstractRetinoic acid-related orphan receptor α (RORα) functions as a transcription factor for various biological processes, including circadian rhythm, cancer, and metabolism. Here, we generate intestinal epithelial cell (IEC)-specific RORα-deficient (RORαΔIEC) mice and find that RORα is crucial for maintaining intestinal homeostasis by attenuating nuclear factor κB (NF-κB) transcriptional activity. RORαΔIEC mice exhibit excessive intestinal inflammation and highly activated inflammatory responses in the dextran sulfate sodium (DSS) mouse colitis model. Transcriptome analysis reveals that deletion of RORα leads to up-regulation of NF-κB target genes in IECs. Chromatin immunoprecipitation analysis reveals corecruitment of RORα and histone deacetylase 3 (HDAC3) on NF-κB target promoters and subsequent dismissal of CREB binding protein (CBP) and bromodomain-containing protein 4 (BRD4) for transcriptional repression. Together, we demonstrate that RORα/HDAC3-mediated attenuation of NF-κB signaling controls the balance of inflammatory responses, and therapeutic strategies targeting this epigenetic regulation could be beneficial to the treatment of chronic inflammatory diseases, including inflammatory bowel disease (IBD).-
dc.description.sponsorshipACKNOWLEDGMENTS. We thank the National Cancer Center Animal Sciences Branch for excellent guidance and assistance with the performed mouse experiments. This work was supported by the Creative Research Initiatives Program (Research Center for Epigenetics Code and Diseases, Grant NRF-2017R1A3B1023387), the Bio & Medical Technology Development Program (Grant NRF-2018M3A9E2023523), and the Science Research Center Program (Grant NRF-2016R1A5A1010764) (all to S.H.B.); Korea Mouse Phenotyping Project Grant 2013M3A9D5072550 and Bio & Medical Technology Development Program Grant 2017M3A9F3046538 (to S.F.); Collaborative Genome Program Grant NRF-2017M3C9A5031595 (to D.P.); National Research Foundation Grant NRF-2019R1C1C1008181 (to D.P.) and Grant NRF-2019R1C1C1004022 (to D.K.); and National Cancer Center Grant NCC-1310100 (to H.L.).-
dc.language.isoeng-
dc.publisherNational Academy of Sciences-
dc.subject.meshAnimals-
dc.subject.meshEpigenesis, Genetic-
dc.subject.meshEpithelial Cells-
dc.subject.meshFemale-
dc.subject.meshHomeostasis-
dc.subject.meshInflammation-
dc.subject.meshIntestines-
dc.subject.meshMice-
dc.subject.meshMice, Inbred C57BL-
dc.subject.meshNF-kappa B-
dc.subject.meshOrphan Nuclear Receptors-
dc.subject.meshTranscription Factors-
dc.subject.meshTranscription, Genetic-
dc.subject.meshTranscriptome-
dc.titleRORα is crucial for attenuated inflammatory response to maintain intestinal homeostasis-
dc.typeArticle-
dc.citation.endPage21149-
dc.citation.number42-
dc.citation.startPage21140-
dc.citation.titleProceedings of the National Academy of Sciences of the United States of America-
dc.citation.volume116-
dc.identifier.bibliographicCitationProceedings of the National Academy of Sciences of the United States of America, Vol.116 No.42, pp.21140-21149-
dc.identifier.doi10.1073/pnas.1907595116-
dc.identifier.pmid31570593-
dc.identifier.scopusid2-s2.0-85073308098-
dc.identifier.urlhttps://www.pnas.org/content/pnas/116/42/21140.full.pdf-
dc.subject.keywordEpigenetic regulation-
dc.subject.keywordHDAC3-
dc.subject.keywordInflammation-
dc.subject.keywordNF-kB signaling-
dc.subject.keywordRORα-
dc.type.otherArticle-
dc.identifier.pissn0027-8424-
dc.description.isoatrue-
dc.subject.subareaMultidisciplinary-
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