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Brefeldin A-sensitive ER-Golgi vesicle trafficking contributes to NLRP3-dependent caspase-1 activation

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dc.contributor.author유제욱-
dc.contributor.author황인화-
dc.date.accessioned2019-05-29T05:10:17Z-
dc.date.available2019-05-29T05:10:17Z-
dc.date.issued2019-
dc.identifier.issn0892-6638-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/169441-
dc.description.abstractEndoplasmic reticulum (ER)-Golgi vesicle trafficking plays a pivotal role in the conventional secretory pathway of many cytokines; however, the precise release mechanism of a major inflammasome mediator, IL-1β, is not thought to follow the conventional ER-Golgi route and remains elusive. Here, we found that perturbation of ER-Golgi trafficking by brefeldin A (BFA) treatment attenuated nucleotide-binding oligomerization domain-like receptor family, pyrin-domain-containing 3 (NLRP3) inflammasome activation in mouse bone marrow-derived macrophages (BMDMs). BFA treatment inhibited NLRP3-mediated inflammasome assembly and caspase-1 activation but did not block IL-1β secretion from BMDMs following BFA administration after NLRP3 inflammasome activation. Consistently, short-hairpin RNA-dependent knockdown of BFA-inhibited guanine nucleotide-exchange protein 1 (BIG1), a molecular target of BFA and an initiator of Golgi-specific vesicle trafficking, abolished NLRP3-dependent apoptosis-associated speck-like protein containing a caspase-recruitment domain oligomerization and caspase-1 activation in BMDMs. Similarly, knockdown of Golgi-specific BFA-resistance guanine nucleotide exchange factor 1, another target of BFA, clearly attenuated NLRP3-mediated caspase-1 activation in BMDMs. Mechanistically, inhibition of BIG1-mediated vesicle trafficking did not impair NLRP3-activating signal 2-promoted events, such as potassium efflux and mitochondrial rearrangement, but caused significant impairment of signal 1-triggered priming steps, including NF-κB-mediated pathways. These data suggest that BFA-targeted vesicle trafficking at the Golgi contributes to activation of the NLRP3 inflammasome signaling.-Hong, S., Hwang, I., Gim, E., Yang, J., Park, S., Yoon, S.-H., Lee, W.-W., Yu, J.-W. Brefeldin A-sensitive ER-Golgi vesicle trafficking contributes to NLRP3-dependent caspase-1 activation.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherThe Federation-
dc.relation.isPartOfFASEB JOURNAL-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleBrefeldin A-sensitive ER-Golgi vesicle trafficking contributes to NLRP3-dependent caspase-1 activation-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Microbiology (미생물학교실)-
dc.contributor.googleauthorSujeong Hong-
dc.contributor.googleauthorInhwa Hwang-
dc.contributor.googleauthorEunji Gim-
dc.contributor.googleauthorJungmin Yang-
dc.contributor.googleauthorSangjun Park-
dc.contributor.googleauthorSung-Hyun Yoon-
dc.contributor.googleauthorWon-Woo Lee-
dc.contributor.googleauthorJe-Wook Yu-
dc.identifier.doi10.1096/fj.201801585R-
dc.contributor.localIdA02508-
dc.contributor.localIdA05445-
dc.contributor.localIdA05445-
dc.relation.journalcodeJ00889-
dc.identifier.eissn1530-6860-
dc.identifier.pmid30592629-
dc.identifier.urlhttps://www.fasebj.org/doi/full/10.1096/fj.201801585R-
dc.subject.keywordBFA-
dc.subject.keywordBIG1-
dc.subject.keywordIL-1β secretion-
dc.subject.keywordinflammasome-
dc.contributor.alternativeNameYu, Je Wook-
dc.contributor.affiliatedAuthor유제욱-
dc.contributor.affiliatedAuthor황인화-
dc.contributor.affiliatedAuthor황인화-
dc.citation.volume33-
dc.citation.number3-
dc.citation.startPage4547-
dc.citation.endPage4558-
dc.identifier.bibliographicCitationFASEB JOURNAL, Vol.33(3) : 4547-4558, 2019-
dc.identifier.rimsid62577-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers

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