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Article: Angiotensin converting enzyme inhibitor but not angiotensin receptor blockade or statin ameliorates murine adriamycin nephropathy

TitleAngiotensin converting enzyme inhibitor but not angiotensin receptor blockade or statin ameliorates murine adriamycin nephropathy
Authors
KeywordsACE inhibitors
Chemokine
Nephropathy
Renal tubular epithelial cells
Issue Date2008
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, 2008, v. 73 n. 3, p. 288-299 How to Cite?
AbstractAngiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and statins have renoprotective effects. We studied the cellular mechanisms for this effect in adriamycin-treated mice receiving captopril, losartan, simvastatin, or their combinations. The mice developed albuminuria, renal insufficiency, and parenchymal inflammation/fibrosis accompanied by overexpression of intrarenal converting enzyme and angiotensin II. Only captopril consistently improved these abnormalities and reduced the cortical expression of several proinflammatory and profibrotic factors including transforming growth factor-β (TGF-β). These effects were independent of blood pressure, accompanied by increased urine N-acetylseryl-aspartyl-lysyl- proline (Ac-SDKP) levels, and the restoration of renal angiotensin-converting enzyme and angiotensin II to baseline levels. Losartan or simvastatin alone or together had no effect, and their addition to captopril did not enhance protection. In vitro, angiotensin II stimulated TGF-β in renal tubular cells via mitogen-activated protein kinase (MAPK) signaling. Captopril or Ac-SDKP suppressed angiotensin II-induced MAPK activation and TGF-β secretion. Angiotensin-converting enzyme inhibition confers renoprotection in adriamycin nephropathy by reducing intrarenal angiotensin II and augmenting Ac-SDKP expression that together attenuate MAPK signaling and its downstream proinflammatory and fibrogenic properties. The addition of receptor blocker and/or statin failed to potentiate such effects. © 2008 International Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/76983
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorEddy, AAen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T07:27:01Z-
dc.date.available2010-09-06T07:27:01Z-
dc.date.issued2008en_HK
dc.identifier.citationKidney International, 2008, v. 73 n. 3, p. 288-299en_HK
dc.identifier.issn0085-2538en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76983-
dc.description.abstractAngiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and statins have renoprotective effects. We studied the cellular mechanisms for this effect in adriamycin-treated mice receiving captopril, losartan, simvastatin, or their combinations. The mice developed albuminuria, renal insufficiency, and parenchymal inflammation/fibrosis accompanied by overexpression of intrarenal converting enzyme and angiotensin II. Only captopril consistently improved these abnormalities and reduced the cortical expression of several proinflammatory and profibrotic factors including transforming growth factor-β (TGF-β). These effects were independent of blood pressure, accompanied by increased urine N-acetylseryl-aspartyl-lysyl- proline (Ac-SDKP) levels, and the restoration of renal angiotensin-converting enzyme and angiotensin II to baseline levels. Losartan or simvastatin alone or together had no effect, and their addition to captopril did not enhance protection. In vitro, angiotensin II stimulated TGF-β in renal tubular cells via mitogen-activated protein kinase (MAPK) signaling. Captopril or Ac-SDKP suppressed angiotensin II-induced MAPK activation and TGF-β secretion. Angiotensin-converting enzyme inhibition confers renoprotection in adriamycin nephropathy by reducing intrarenal angiotensin II and augmenting Ac-SDKP expression that together attenuate MAPK signaling and its downstream proinflammatory and fibrogenic properties. The addition of receptor blocker and/or statin failed to potentiate such effects. © 2008 International Society of Nephrology.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.htmlen_HK
dc.relation.ispartofKidney Internationalen_HK
dc.subjectACE inhibitorsen_HK
dc.subjectChemokineen_HK
dc.subjectNephropathyen_HK
dc.subjectRenal tubular epithelial cellsen_HK
dc.subject.meshAngiotensin II - metabolismen_HK
dc.subject.meshAngiotensin II Type 1 Receptor Blockers - pharmacology - therapeutic useen_HK
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - pharmacology - therapeutic useen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Proliferation - drug effectsen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshChemokine CCL2 - metabolismen_HK
dc.subject.meshCollagen Type I - metabolismen_HK
dc.subject.meshDoxorubicin - adverse effectsen_HK
dc.subject.meshDrug Therapy, Combinationen_HK
dc.subject.meshEpithelial Cells - drug effectsen_HK
dc.subject.meshGlomerulosclerosis, Focal Segmental - drug therapy - metabolism - pathologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology - therapeutic useen_HK
dc.subject.meshKidney - drug effects - immunology - metabolism - pathologyen_HK
dc.subject.meshMacrophages - drug effectsen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshPeptidyl-Dipeptidase A - metabolismen_HK
dc.subject.meshPhenotypeen_HK
dc.subject.meshPregnancy Proteins - metabolismen_HK
dc.subject.meshSignal Transduction - drug effectsen_HK
dc.subject.meshTransforming Growth Factor beta - metabolismen_HK
dc.titleAngiotensin converting enzyme inhibitor but not angiotensin receptor blockade or statin ameliorates murine adriamycin nephropathyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0085-2538&volume=73&spage=288&epage=299&date=2008&atitle=Angiotensin+converting+enzyme+inhibitor+but+not+angiotensin+receptor+blockade+or+statin+ameliorates+murine+adriamycin+nephropathyen_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.ki.5002674en_HK
dc.identifier.pmid18033243-
dc.identifier.scopuseid_2-s2.0-38149125631en_HK
dc.identifier.hkuros140283en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-38149125631&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume73en_HK
dc.identifier.issue3en_HK
dc.identifier.spage288en_HK
dc.identifier.epage299en_HK
dc.identifier.eissn1523-1755-
dc.identifier.isiWOS:000252388300008-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridChan, LYY=55182644100en_HK
dc.identifier.scopusauthoridEddy, AA=25932921000en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

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