DC Field | Value | Language |
---|---|---|
dc.contributor.author | Hajeong Lee | - |
dc.contributor.author | Jae Wook Lee | - |
dc.contributor.author | Kyung Don Yoo | - |
dc.contributor.author | Yoo, JY | - |
dc.contributor.author | Jung Pyo Lee | - |
dc.contributor.author | Dong Ki Kim | - |
dc.contributor.author | Ho Jun Chin | - |
dc.contributor.author | Yon Su Kim | - |
dc.contributor.author | Seung Hee Yang | - |
dc.date.accessioned | 2017-07-19T13:43:02Z | - |
dc.date.available | 2017-07-19T13:43:02Z | - |
dc.date.created | 2016-09-09 | - |
dc.date.issued | 2016-09-01 | - |
dc.identifier.issn | 1931-857X | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/37446 | - |
dc.description.abstract | T helper 17 (Th17) lymphocytes promote renal inflammation in antiglomerular basement membrane glomerulonephritis (anti-GBM GN), and signal transducer and activator of transcription 3 (STAT3) mediates activation of Th17 lymphocytes by IL-6 and transforming growth factor-beta (TGF-beta). Cln 3-requiring 9 (Ctr9), a subunit of RNA polymerase-associated factor complex (PAFc), regulates the transcription of IL-6/STAT3-dependent genes. Here, we investigated the role of Ctr9 in regulating Th17-driven inflammation in anti-GBM GN. In mice, STAT3 beta or IL-17 knockout ameliorated anti-GBM autoantibody-induced renal injury. This phenomenon was associated with decreases in retinoic acid receptor-related orphan receptor gamma t (ROR gamma t), IL-17, phosphorylated STAT3, and proinflammatory cytokines. Compared with wild-type mice, Ctr9 increased in both STAT3 beta(-/-) and IL-17(-/-) mice injected with anti-GBM IgG, showing a negative correlation with Th17-related transcripts. Small interfering RNA (siRNA)-mediated knockdown of Ctr9 in intrarenal lymphocytes further upregulated Th17-related transcripts, consistent with repression of Th17 differentiation by Ctr9. Interestingly, Ctr9 was also expressed in human and mouse mesangial cells and downregulated in response to anti-GBM IgG or to TGF-beta plus IL-17. Ctr9 in mesangial cells was even more repressed in the presence of both anti-GBM IgG and Th17-activating cytokines. Consistent with these findings, renal biopsies obtained from patients with anti-GBM GN showed consistent downregulation of Ctr9 and upregulation of phosphorylated STAT3 and IL-17 in the glomerulus. We conclude that Ctr9 is a negative regulator of Th17 differentiation in anti-GBM GN and repressed by anti-GBM IgG and IL-17 in mesangial cells. | - |
dc.language | English | - |
dc.publisher | Bethesda, Md. : American Physiological Society | - |
dc.relation.isPartOf | AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY | - |
dc.title | Cln 3-requiring 9 is a negative regulator of Th17 pathway-driven inflammation in anti-glomerular basement membrane glomerulonephritis | - |
dc.type | Article | - |
dc.identifier.doi | 10.1152/AJPRENAL.00533.2015 | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, v.311, no.3, pp.F505 - 19 | - |
dc.identifier.wosid | 000384977500003 | - |
dc.date.tcdate | 2019-02-01 | - |
dc.citation.endPage | 19 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | F505 | - |
dc.citation.title | AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY | - |
dc.citation.volume | 311 | - |
dc.contributor.affiliatedAuthor | Yoo, JY | - |
dc.identifier.scopusid | 2-s2.0-84986218306 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.wostc | 2 | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | RNA-POLYMERASE-II | - |
dc.subject.keywordPlus | PAF1 COMPLEX | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | T-CELLS | - |
dc.subject.keywordPlus | CRESCENTIC GLOMERULONEPHRITIS | - |
dc.subject.keywordPlus | FACTOR STAT3 | - |
dc.subject.keywordPlus | ROR-GAMMA | - |
dc.subject.keywordPlus | TRANSCRIPTION | - |
dc.subject.keywordPlus | BETA | - |
dc.subject.keywordPlus | DIFFERENTIATION | - |
dc.subject.keywordAuthor | anti-glomerular basement membrane glomerulonephritis | - |
dc.subject.keywordAuthor | Ctr9 | - |
dc.subject.keywordAuthor | STAT3 | - |
dc.subject.keywordAuthor | Th17 pathway | - |
dc.relation.journalWebOfScienceCategory | Physiology | - |
dc.relation.journalWebOfScienceCategory | Urology & Nephrology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Physiology | - |
dc.relation.journalResearchArea | Urology & Nephrology | - |
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