DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Kyung-Hyun | ko |
dc.contributor.author | Hong, Geum-Lan | ko |
dc.contributor.author | Jung, Da-Young | ko |
dc.contributor.author | Karunasagara, Shanika | ko |
dc.contributor.author | Jeong, Won-Il | ko |
dc.contributor.author | Jung, Ju-Young | ko |
dc.date.accessioned | 2021-04-20T05:10:12Z | - |
dc.date.available | 2021-04-20T05:10:12Z | - |
dc.date.created | 2021-04-19 | - |
dc.date.created | 2021-04-19 | - |
dc.date.created | 2021-04-19 | - |
dc.date.issued | 2021-03 | - |
dc.identifier.citation | MOLECULAR MEDICINE, v.27, no.1 | - |
dc.identifier.issn | 1076-1551 | - |
dc.identifier.uri | http://hdl.handle.net/10203/282479 | - |
dc.description.abstract | BackgroundDiabetic nephropathy (DN) is one of the most important medical complications of diabetes mellitus. Autophagy is an important mediator of pathological response and plays a critical role in inflammation during the progression of diabetic nephropathy. Interleukin (IL)-17A favorably modulates inflammatory disorders including DN. In this study, we examined whether IL-17A deficiency affected the autophagy process in the kidneys of mice with streptozotocin (STZ)-induced DN.MethodsThe autophagic response of IL-17A to STZ-induced nephrotoxicity was evaluated by analyzing STZ-induced functional and histological renal injury in IL-17A knockout (KO) mice.ResultsIL-17A KO STZ-treated mice developed more severe nephropathy than STZ-treated wild-type (WT) mice, with increased glomerular damage and renal interstitial fibrosis at 12 weeks. IL-17A deficiency also increased the up-regulation of proinflammatory cytokines and fibrotic gene expression after STZ treatment. Meanwhile, autophagy-associated proteins were induced in STZ-treated WT mice. However, IL-17A KO STZ-treated mice displayed a significant decrease in protein expression. Especially, the levels of LC3 and ATG7, which play crucial roles in autophagosome formation, were notably decreased in the IL-17A KO STZ-treated mice compared with their WT counterparts.ConclusionsIL-17 deficiency aggravates of STZ-induced DN via attenuation of autophagic response. Our study demonstrated that IL-17A mediates STZ-induced renal damage and represents a potential therapeutic target in DN. | - |
dc.language | English | - |
dc.publisher | SPRINGER | - |
dc.title | IL-17 deficiency aggravates the streptozotocin-induced diabetic nephropathy through the reduction of autophagosome formation in mice | - |
dc.type | Article | - |
dc.identifier.wosid | 000627814800003 | - |
dc.identifier.scopusid | 2-s2.0-85102240494 | - |
dc.type.rims | ART | - |
dc.citation.volume | 27 | - |
dc.citation.issue | 1 | - |
dc.citation.publicationname | MOLECULAR MEDICINE | - |
dc.identifier.doi | 10.1186/s10020-021-00285-4 | - |
dc.contributor.localauthor | Jeong, Won-Il | - |
dc.contributor.nonIdAuthor | Kim, Kyung-Hyun | - |
dc.contributor.nonIdAuthor | Hong, Geum-Lan | - |
dc.contributor.nonIdAuthor | Jung, Da-Young | - |
dc.contributor.nonIdAuthor | Karunasagara, Shanika | - |
dc.contributor.nonIdAuthor | Jung, Ju-Young | - |
dc.description.isOpenAccess | Y | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | IL-17A | - |
dc.subject.keywordAuthor | Diabetic nephropathy | - |
dc.subject.keywordAuthor | Autophagy | - |
dc.subject.keywordAuthor | Autophagosome formation | - |
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