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The protective role of uteroglobin through the modulation of tissue transglutaminase in the experimental crescentic glomerulonephritis

Cited 8 time in Web of Science Cited 8 time in Scopus
Authors
Yang, Seung Hee; Shin, Sung Joon; Oh, Ji Eun; Jin, Ji Zhe; Chung, Nam Hyun; Lim, Chun Soo; Kim, Suhnggwon; Kim, Yon Su
Issue Date
2008-06-19
Publisher
Oxford University Press
Citation
Nephrol Dial Transplant. 2008 ;23(11):3437-3445.
Keywords
AnimalsAntibodies, Anti-IdiotypicCell Line, TumorCell Proliferation/drug effectsCells, CulturedDisease Models, AnimalGlomerulonephritis/chemically induced/*metabolism/pathologyHumansMesangial Cells/drug effects/*metabolism/pathologyMiceMice, Inbred C57BLRecombinant Proteins/pharmacologySeverity of Illness IndexTransforming Growth Factor beta1/metabolismTransglutaminases/*metabolismUteroglobin/*pharmacology
Abstract
BACKGROUND AND METHODS: Tissue transglutaminase (tTG) may induce pro-inflammatory cytokines and produce irreversible end-products, thus promoting renal scarring. It has recently been confirmed that the crescent formation in murine experimental crescentic glomerulonephritis (ecGN) has been inhibited by the administration of recombinant uteroglobin (rUG). However, the ability of UG on tTG modulation has not been thoroughly assessed. In this study, we investigated the feasible protective role of UG in murine ecGN through the modulation of tTG and TGF-beta1 expressions. ecGN was induced by the administration of anti-GBM Ab into C57BL/6 mice. RESULTS: Both proteinuria and BUN levels were distinctively lower in rUG-treated mice compared to those of disease control mice. Glomerular injuries such as mesangial proliferation, matrix production and crescent formation were lessened with the rUG treatment, and these findings were parallel with the attenuated expression of tTG and TGF-beta1. tTG and TGF-beta1 were expressed mainly on mesangial areas by the induction of ecGN and rUG treatment markedly attenuated the expressions of these proteins in glomeruli without spatial changes. With the addition of LPS to mesangial cells, the expressions of tTG and TGF-beta1 were up-regulated, whilst the addition of cysteamine, tTG inhibitor, attenuated the expression of tTG and TGF-beta1 as well as the cellular proliferation which was further induced by LPS. CONCLUSION: We demonstrate for the first time that rUG is able to attenuate the renal injury through the modulation of expressions of tTG and TGF-beta1 in ecGN and further suggest a wide range of feasible molecular targets to reduce the severity of human glomerulonephritis.
ISSN
1460-2385 (Electronic)
Language
English
URI
http://hdl.handle.net/10371/62217
DOI
https://doi.org/10.1093/ndt/gfn268
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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