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Article: Renoprotection by Rosiglitazone in Accelerated Type 2 Diabetic Nephropathy: Role of STAT1 Inhibition and Nephrin Restoration

TitleRenoprotection by Rosiglitazone in Accelerated Type 2 Diabetic Nephropathy: Role of STAT1 Inhibition and Nephrin Restoration
Authors
Issue Date2010
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/AJN
Citation
American Journal Of Nephrology, 2010, v. 32 n. 2, p. 145-155 How to Cite?
AbstractBackground: Rosiglitazone (Ros) has been shown to attenuate CXCL8 and ICAM-1 overexpression in renal tubular cells exposed to glycated albumin. The present study explores whether this can be translated into renoprotection in vivo. Uninephrectomized (Unx) type 2 diabetic db/db mice were chosen as a model of accelerated diabetic nephropathy. Methods: Uninephrectomy was performed in 10-week-old db/db mice. They were then treated with vehicle, metformin or Ros for 8 weeks. Results: Unx-db/db mice treated with Ros had lower serum creatinine and albuminuria, less severe glomerulosclerosis, tubulointerstitial injury, fewer infiltrating macrophages, and less proliferating nuclear antigen-positive tubular cells compared with mice treated with metformin that had a similar level of glycemic control and insulin resistance. In addition, Ros but not metformin attenuated renal cortical expression of CCL2, MIP-2, and ICAM-1 and inhibited p-STAT1 signal activation. Ros also increased glomerular nephrin expression. Conclusions: Our results delineated the biochemical and histologic characteristics of Unx-db/db mice and demonstrated the in vivo glucose-independent anti-inflammatory mechanisms of Ros in nephropathy of accelerated murine type 2 diabetes. Copyright © 2010 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/125077
ISSN
2014 Impact Factor: 2.669
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong KongHKU 7764/07M
Funding Information:

This study is supported by a General Research Fund of the Research Grants Council (Grant No. HKU 7764/07M) of Hong Kong. Rosiglitazone was a kind gift from GlaxoSmithKline (Compound Management Division, Stevenage, UK).

 

DC FieldValueLanguage
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorCheng, ASen_HK
dc.contributor.authorLan, HYen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-10-31T11:10:06Z-
dc.date.available2010-10-31T11:10:06Z-
dc.date.issued2010en_HK
dc.identifier.citationAmerican Journal Of Nephrology, 2010, v. 32 n. 2, p. 145-155en_HK
dc.identifier.issn0250-8095en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125077-
dc.description.abstractBackground: Rosiglitazone (Ros) has been shown to attenuate CXCL8 and ICAM-1 overexpression in renal tubular cells exposed to glycated albumin. The present study explores whether this can be translated into renoprotection in vivo. Uninephrectomized (Unx) type 2 diabetic db/db mice were chosen as a model of accelerated diabetic nephropathy. Methods: Uninephrectomy was performed in 10-week-old db/db mice. They were then treated with vehicle, metformin or Ros for 8 weeks. Results: Unx-db/db mice treated with Ros had lower serum creatinine and albuminuria, less severe glomerulosclerosis, tubulointerstitial injury, fewer infiltrating macrophages, and less proliferating nuclear antigen-positive tubular cells compared with mice treated with metformin that had a similar level of glycemic control and insulin resistance. In addition, Ros but not metformin attenuated renal cortical expression of CCL2, MIP-2, and ICAM-1 and inhibited p-STAT1 signal activation. Ros also increased glomerular nephrin expression. Conclusions: Our results delineated the biochemical and histologic characteristics of Unx-db/db mice and demonstrated the in vivo glucose-independent anti-inflammatory mechanisms of Ros in nephropathy of accelerated murine type 2 diabetes. Copyright © 2010 S. Karger AG, Basel.en_HK
dc.languageengen_HK
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.rightsAmerican Journal of Nephrology. Copyright © S Karger AG.-
dc.subject.meshAnti-Inflammatory Agents - pharmacology-
dc.subject.meshDiabetes Mellitus, Type 2 - complications-
dc.subject.meshDiabetic Nephropathies - metabolism - pathology - prevention and control-
dc.subject.meshMembrane Proteins - biosynthesis - genetics-
dc.subject.meshProtective Agents - pharmacology-
dc.titleRenoprotection by Rosiglitazone in Accelerated Type 2 Diabetic Nephropathy: Role of STAT1 Inhibition and Nephrin Restorationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0250-8095&volume=32&issue=2&spage=145&epage=155&date=2010&atitle=Renoprotection+by+rosiglitazone+in+accelerated+type+2+diabetic+nephropathy:+role+of+STAT1+inhibition+and+nephrin+restorationen_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.doi10.1159/000316056en_HK
dc.identifier.pmid20606418-
dc.identifier.scopuseid_2-s2.0-77954207147en_HK
dc.identifier.hkuros173996en_HK
dc.identifier.volume32en_HK
dc.identifier.issue2en_HK
dc.identifier.spage145en_HK
dc.identifier.epage155en_HK
dc.identifier.isiWOS:000280476600007-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridChan, LYY=55182644100en_HK
dc.identifier.scopusauthoridCheng, AS=7402075136en_HK
dc.identifier.scopusauthoridLan, HY=24544799000en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.citeulike7898113-

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