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Article: Rapamycin attenuates the severity of murine adriamycin nephropathy

TitleRapamycin attenuates the severity of murine adriamycin nephropathy
Authors
KeywordsFocal segmental glomerulosclerosis
Glomerulosclerosis
Interstitial fibrosis
Proteinuria
Issue Date2009
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/AJN
Citation
American Journal Of Nephrology, 2009, v. 29 n. 4, p. 342-352 How to Cite?
AbstractBackground: Rapamycin is an immunosuppressive drug with potent antifibrotic activity. We evaluated the effect of rapamycin on murine adriamycin nephropathy, a model of progressive glomerulosclerosis and tubulointerstitial fibrosis. Methods: Adriamycin nephropathy was induced in Balb/c mice by a single intravenous injection of adriamycin. The mice were treated orally with either saline or rapamycin, beginning at the time of adriamycin injection or rapamycin starting 1 week after adriamycin injection. The mice were sacrificed 6 weeks after adriamycin injection. Results: Saline-treated mice developed massive proteinuria and impaired renal function. Kidney sections from saline-treated mice showed marked focal segmental glomerulosclerosis, tubular dilation with protein cast deposition, interstitial fibrosis, and numerous infiltrating macrophages and T lymphocytes. The intrarenal expression of Collagen I and RANTES was also increased. In contrast, both groups of rapamycin-treated mice had markedly reduced proteinuria and preserved renal function, with only mild histological abnormalities. The intrarenal expression of Collagen I and RANTES was reduced, concomitant with a significant reduction in interstitial inflammatory cell infiltration. Conclusions: Rapamycin is effective in attenuating the glomerular and tubulointerstitial abnormalities in adriamycin nephropathy.The beneficial effects of rapamycin are mediated, at least in part, through reduced RANTES expression and inflammatory cell infiltration. © 2008 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/148587
ISSN
2015 Impact Factor: 2.605
2015 SCImago Journal Rankings: 1.308
ISI Accession Number ID
Funding AgencyGrant Number
RGC Competitive Earmarked ResearchHKU7550/06M
Hong Kong Society of Nephrology
Hong Kong Kidney Foundation
Wai Hung Charity Foundation
Funding Information:

This study was supported by research grants from the RGC Competitive Earmarked Research Grant (HKU7550/06M), the Hong Kong Society of Nephrology, the Hong Kong Kidney Foundation, and the Wai Hung Charity Foundation. The donors had no role in the study design and execution, data analysis and interpretation, or writing of the report.

References

 

DC FieldValueLanguage
dc.contributor.authorLui, SLen_HK
dc.contributor.authorTsang, Ren_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorZhang, Fen_HK
dc.contributor.authorTam, Sen_HK
dc.contributor.authorYung, Sen_HK
dc.contributor.authorChan, TMen_HK
dc.date.accessioned2012-05-29T06:13:55Z-
dc.date.available2012-05-29T06:13:55Z-
dc.date.issued2009en_HK
dc.identifier.citationAmerican Journal Of Nephrology, 2009, v. 29 n. 4, p. 342-352en_HK
dc.identifier.issn0250-8095en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148587-
dc.description.abstractBackground: Rapamycin is an immunosuppressive drug with potent antifibrotic activity. We evaluated the effect of rapamycin on murine adriamycin nephropathy, a model of progressive glomerulosclerosis and tubulointerstitial fibrosis. Methods: Adriamycin nephropathy was induced in Balb/c mice by a single intravenous injection of adriamycin. The mice were treated orally with either saline or rapamycin, beginning at the time of adriamycin injection or rapamycin starting 1 week after adriamycin injection. The mice were sacrificed 6 weeks after adriamycin injection. Results: Saline-treated mice developed massive proteinuria and impaired renal function. Kidney sections from saline-treated mice showed marked focal segmental glomerulosclerosis, tubular dilation with protein cast deposition, interstitial fibrosis, and numerous infiltrating macrophages and T lymphocytes. The intrarenal expression of Collagen I and RANTES was also increased. In contrast, both groups of rapamycin-treated mice had markedly reduced proteinuria and preserved renal function, with only mild histological abnormalities. The intrarenal expression of Collagen I and RANTES was reduced, concomitant with a significant reduction in interstitial inflammatory cell infiltration. Conclusions: Rapamycin is effective in attenuating the glomerular and tubulointerstitial abnormalities in adriamycin nephropathy.The beneficial effects of rapamycin are mediated, at least in part, through reduced RANTES expression and inflammatory cell infiltration. © 2008 S. Karger AG, Basel.en_HK
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/AJNen_HK
dc.relation.ispartofAmerican Journal of Nephrologyen_HK
dc.subjectFocal segmental glomerulosclerosisen_HK
dc.subjectGlomerulosclerosisen_HK
dc.subjectInterstitial fibrosisen_HK
dc.subjectProteinuriaen_HK
dc.subject.meshAlbuminuria - Chemically Induced - Drug Therapy - Immunologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntibiotics, Antineoplastic - Toxicityen_US
dc.subject.meshBody Weighten_US
dc.subject.meshChemokine Ccl5 - Geneticsen_US
dc.subject.meshCollagen Type I - Geneticsen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshDoxorubicin - Toxicityen_US
dc.subject.meshFibrosisen_US
dc.subject.meshGene Expression - Drug Effects - Immunologyen_US
dc.subject.meshGlomerulosclerosis, Focal Segmental - Chemically Induced - Drug Therapy - Immunologyen_US
dc.subject.meshImmunosuppressive Agents - Pharmacologyen_US
dc.subject.meshKidney - Immunology - Pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Balb Cen_US
dc.subject.meshSeverity Of Illness Indexen_US
dc.subject.meshSirolimus - Pharmacologyen_US
dc.subject.meshSurvival Rateen_US
dc.titleRapamycin attenuates the severity of murine adriamycin nephropathyen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, KW:hrmtckw@hku.hken_HK
dc.identifier.emailYung, S:ssyyung@hku.hken_HK
dc.identifier.emailChan, TM:dtmchan@hku.hken_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityYung, S=rp00455en_HK
dc.identifier.authorityChan, TM=rp00394en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1159/000166599en_HK
dc.identifier.pmid18948688-
dc.identifier.scopuseid_2-s2.0-54249094189en_HK
dc.identifier.hkuros157927en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-54249094189&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue4en_HK
dc.identifier.spage342en_HK
dc.identifier.epage352en_HK
dc.identifier.isiWOS:000261132100008-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridLui, SL=7102379130en_HK
dc.identifier.scopusauthoridTsang, R=7102940073en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridZhang, F=25522980800en_HK
dc.identifier.scopusauthoridTam, S=7202037323en_HK
dc.identifier.scopusauthoridYung, S=22636568800en_HK
dc.identifier.scopusauthoridChan, TM=7402687700en_HK

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