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HDAC11 Regulates Palmitate-induced NLRP3 Inflammasome Activation by Inducing YAP Expression in THP-1 Cells and PBMCs

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dc.contributor.authorByeon, HE-
dc.contributor.authorChoi, SE-
dc.contributor.authorKim, Y-
dc.contributor.authorChoi, S-
dc.contributor.authorLee, SJ-
dc.contributor.authorKim, DH-
dc.contributor.authorMo, JS-
dc.contributor.authorJeon, JY-
dc.date.accessioned2024-03-14T04:52:41Z-
dc.date.available2024-03-14T04:52:41Z-
dc.date.issued2024-
dc.identifier.issn0013-7227-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/32359-
dc.description.abstractHistone deacetylase 11 (HDAC11) has been implicated in the pathogenesis of metabolic diseases characterized by chronic low-grade inflammation, such as obesity. However, the influence of HDAC11 on inflammation and the specific effect of HDAC11 on the palmitic acid (PA)-induced NLR family pyrin domain containing 3 (NLRP3) inflammasome activation are poorly understood. The effect of PA treatment on HDAC11 activity and the NLRP3 inflammasome was investigated in human peripheral blood mononuclear cells and THP-1 cells. The PA-induced responses of key markers of NLRP3 inflammasome activation, including NLRP3 gene expression, caspase-1 p10 activation, cleaved IL-1β production, and extracellular IL-1β release, were assessed as well. The role of HDAC11 was explored using a specific inhibitor of HDAC11 and by knockdown using small interfering (si)HDAC11 RNA. The relationship between HDAC11 and yes-associated protein (YAP) in the PA-induced NLRP3 inflammasome was investigated in THP-1 cells with HDAC11 or YAP knockdown. Following PA treatment, HDAC11 activity and protein levels increased significantly, concomitant with activation of the NLRP3 inflammasome. Notably, PA-induced the upregulation of NLRP3, caspase-1 p10 activation, the production of cleaved IL-1β, and the release of IL-1β into the extracellular space, all of which were attenuated by FT895 treatment and by HDAC11 knockdown. In THP-1 cells, PA induced the expression of YAP and its interaction with NLRP3, resulting in NLRP3 inflammasome activation, whereas both were inhibited by FT895 and siHDAC11 RNA. These findings demonstrate a pivotal role for HDAC11 in the PA-induced activation of the NLRP3 inflammasome. HDAC11 inhibition thus represents a promising therapeutic strategy for mitigating NLRP3 inflammasome-related inflammation in the context of obesity.-
dc.language.isoen-
dc.subject.MESHCaspase 1-
dc.subject.MESHHistone Deacetylases-
dc.subject.MESHHumans-
dc.subject.MESHInflammasomes-
dc.subject.MESHInflammation-
dc.subject.MESHInterleukin-1beta-
dc.subject.MESHLeukocytes, Mononuclear-
dc.subject.MESHNLR Family, Pyrin Domain-Containing 3 Protein-
dc.subject.MESHObesity-
dc.subject.MESHPalmitates-
dc.subject.MESHPalmitic Acid-
dc.subject.MESHRNA-
dc.subject.MESHYAP-Signaling Proteins-
dc.titleHDAC11 Regulates Palmitate-induced NLRP3 Inflammasome Activation by Inducing YAP Expression in THP-1 Cells and PBMCs-
dc.typeArticle-
dc.identifier.pmid38366363-
dc.subject.keywordHDAC11-
dc.subject.keywordinflammasome-
dc.subject.keywordNLRP3-
dc.subject.keywordpalmitate-
dc.subject.keywordYAP-
dc.contributor.affiliatedAuthorByeon, HE-
dc.contributor.affiliatedAuthorChoi, SE-
dc.contributor.affiliatedAuthorMo, JS-
dc.contributor.affiliatedAuthorJeon, JY-
dc.type.localJournal Papers-
dc.identifier.doi10.1210/endocr/bqae011-
dc.citation.titleEndocrinology-
dc.citation.volume165-
dc.citation.number3-
dc.citation.date2024-
dc.citation.startPagebqae011-
dc.citation.endPagebqae011-
dc.identifier.bibliographicCitationEndocrinology, 165(3). : bqae011-bqae011, 2024-
dc.embargo.liftdate9999-12-31-
dc.embargo.terms9999-12-31-
dc.identifier.eissn1945-7170-
dc.relation.journalidJ000137227-
Appears in Collections:
Journal Papers > Research Organization > Institute for Medical Sciences
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
Journal Papers > School of Medicine / Graduate School of Medicine > Endocrinology & Metabolism
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