Cited 28 times in
Klotho plays a protective role against glomerular hypertrophy in a cell cycle-dependent manner in diabetic nephropathy
DC Field | Value | Language |
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dc.contributor.author | 강신욱 | - |
dc.contributor.author | 박정탁 | - |
dc.contributor.author | 유태현 | - |
dc.contributor.author | 한승혁 | - |
dc.date.accessioned | 2018-10-22T13:15:34Z | - |
dc.date.available | 2018-10-22T13:15:34Z | - |
dc.date.issued | 2018 | - |
dc.identifier.issn | 1931-857X | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/163672 | - |
dc.description.abstract | There are few studies on the effect of klotho on podocytes in diabetic nephropathy. Thus, we tested whether klotho exerts a protective effect against glomerular injury in diabetes. Mouse podocytes were cultured in media containing 5.6 or 30 mM glucose(HG) with or without 200 pM of recombinant klotho (rKL). Additionally, 32 mice were injected intraperitoneally with either diluent( n = 16, C) or with streptozotocin ( n = 16, DM). Control and diabetic mice underwent sham operation and unilateral nephrectomy, respectively. Eight mice from each control and DM group were treated daily with 10 μg·kg-1·day-1 of rKL, using an osmotic minipump. Klotho was expressed in podocytes, and its expression was dependent on peroxisome proliferator-activateed receptor-γ (PPARγ). HG treatment increased the expression of cell cycle-related and apoptotic markers, and these were significantly attenuated by rKL; rKL inhibited the extracellular signal-regulated protein kinase-1/2 and p38 signaling pathways in HG-induced podocyte injury. However, siRNA against klotho gene in HG-treated podocytes failed to aggravate cell cycle arrest and apoptosis. When HG-treated podocytes were incubated in the high-klotho-conditioned medium from tubular epithelial cells, cell injury was significantly attenuated. This effect was not observed when klotho was inhibited by siRNA. In vivo, the expressions of cell cycle-related and apoptotic markers were increased in diabetic mice compared with controls, which were significantly decreased by rKL. Glomerular hypertrophy (GH) and increased profibrotic markers were significantly alleviated after rKL administration. These results showed that klotho was expressed in glomerular podocytes that and its expression was regulated by PPARγ. Additionally, administration of rKL attenuated GH via a cell cycle-dependent mechanism and decreased apoptosis. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | American Physiological Society | - |
dc.relation.isPartOf | AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | Klotho plays a protective role against glomerular hypertrophy in a cell cycle-dependent manner in diabetic nephropathy | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Internal Medicine | - |
dc.contributor.googleauthor | Hyung Jung Oh | - |
dc.contributor.googleauthor | Bo Young Nam | - |
dc.contributor.googleauthor | Meiyan Wu | - |
dc.contributor.googleauthor | Seonghun Kim | - |
dc.contributor.googleauthor | Jimin Park | - |
dc.contributor.googleauthor | Sukyung Kang | - |
dc.contributor.googleauthor | Jung Tak Park | - |
dc.contributor.googleauthor | Tae-Hyun Yoo | - |
dc.contributor.googleauthor | Shin-Wook Kang | - |
dc.contributor.googleauthor | Seung Hyeok Han | - |
dc.identifier.doi | 10.1152/ajprenal.00462.2017 | - |
dc.contributor.localId | A00053 | - |
dc.contributor.localId | A01654 | - |
dc.contributor.localId | A02526 | - |
dc.contributor.localId | A04304 | - |
dc.relation.journalcode | J00108 | - |
dc.identifier.eissn | 1522-1466 | - |
dc.identifier.pmid | 29638159 | - |
dc.identifier.url | https://www.physiology.org/doi/abs/10.1152/ajprenal.00462.2017 | - |
dc.subject.keyword | diabetic nephropathy | - |
dc.subject.keyword | klotho | - |
dc.subject.keyword | peroxisome proliferator-activated receptor-γ | - |
dc.subject.keyword | podocytes | - |
dc.contributor.alternativeName | Kang, Shin Wook | - |
dc.contributor.alternativeName | Park, Jung Tak | - |
dc.contributor.alternativeName | Yoo, Tae Hyun | - |
dc.contributor.alternativeName | Han, Seung Hyeok | - |
dc.contributor.affiliatedAuthor | Kang, Shin Wook | - |
dc.contributor.affiliatedAuthor | Park, Jung Tak | - |
dc.contributor.affiliatedAuthor | Yoo, Tae Hyun | - |
dc.contributor.affiliatedAuthor | Han, Seung Hyeok | - |
dc.citation.volume | 315 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 791 | - |
dc.citation.endPage | 805 | - |
dc.identifier.bibliographicCitation | AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, Vol.315(4) : 791-805, 2018 | - |
dc.identifier.rimsid | 58972 | - |
dc.type.rims | ART | - |
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