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Article: Renoprotection by Rosiglitazone in Accelerated Type 2 Diabetic Nephropathy: Role of STAT1 Inhibition and Nephrin Restoration
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TitleRenoprotection by Rosiglitazone in Accelerated Type 2 Diabetic Nephropathy: Role of STAT1 Inhibition and Nephrin Restoration
 
AuthorsTang, SCW1
Leung, JCK
Chan, LYY
Cheng, AS
Lan, HY
Lai, KN
 
Issue Date2010
 
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/AJN
 
CitationAmerican Journal Of Nephrology, 2010, v. 32 n. 2, p. 145-155 [How to Cite?]
DOI: http://dx.doi.org/10.1159/000316056
 
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.
 
ISSN0250-8095
2013 Impact Factor: 2.646
 
DOIhttp://dx.doi.org/10.1159/000316056
 
ISI Accession Number IDWOS:000280476600007
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 FieldValue
dc.contributor.authorTang, SCW
 
dc.contributor.authorLeung, JCK
 
dc.contributor.authorChan, LYY
 
dc.contributor.authorCheng, AS
 
dc.contributor.authorLan, HY
 
dc.contributor.authorLai, KN
 
dc.date.accessioned2010-10-31T11:10:06Z
 
dc.date.available2010-10-31T11:10:06Z
 
dc.date.issued2010
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationAmerican Journal Of Nephrology, 2010, v. 32 n. 2, p. 145-155 [How to Cite?]
DOI: http://dx.doi.org/10.1159/000316056
 
dc.identifier.citeulike7898113
 
dc.identifier.doihttp://dx.doi.org/10.1159/000316056
 
dc.identifier.epage155
 
dc.identifier.hkuros173996
 
dc.identifier.isiWOS:000280476600007
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.identifier.issn0250-8095
2013 Impact Factor: 2.646
 
dc.identifier.issue2
 
dc.identifier.openurl
 
dc.identifier.pmid20606418
 
dc.identifier.scopuseid_2-s2.0-77954207147
 
dc.identifier.spage145
 
dc.identifier.urihttp://hdl.handle.net/10722/125077
 
dc.identifier.volume32
 
dc.languageeng
 
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/AJN
 
dc.publisher.placeSwitzerland
 
dc.relation.ispartofAmerican Journal of Nephrology
 
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 Restoration
 
dc.typeArticle
 
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<contributor.author>Leung, JCK</contributor.author>
<contributor.author>Chan, LYY</contributor.author>
<contributor.author>Cheng, AS</contributor.author>
<contributor.author>Lan, HY</contributor.author>
<contributor.author>Lai, KN</contributor.author>
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<description.abstract>Background: 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 &#169; 2010 S. Karger AG, Basel.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong