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Angiotensinogen Expression Is Enhanced in the Progression of Glomerular Disease.
MedLine Citation:
PMID:  22247811     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Intrarenal renin-angiotensin system (RAS) activation plays a critical role in the development and progression of renal injury. In the kidney, all of the RAS components are present and intrarenal angiotensin II (Ang II) is formed by multiple independent mechanisms. Angiotensinogen (AGT) is the only known substrate for renin that is a rate-limiting enzyme of the RAS. Recently, enhanced intrarenal AGT levels have been shown to reflect the intrarenal RAS status in hypertension, chronic glomerular disease and diabetic nephropathy. In this review, we focus on AGT expression of the diseased glomeruli in the progression of glomerular disease. An anti-glomerular basement membrane nephritis rat model developed progressive proteinuria and glomerular crescent formation, accompanied by increased macrophage infiltration and glomerular expression of AGT and Ang II. The addition of Ang II type 1 receptor blocker to CC-chemokine recaptor 2 antagonist markedly attenuated the induction of macrophage infiltration, AGT and Ang II, and reduced glomerular crescent formation. Next, the levels of glomerular AGT expression and marker of reactive oxygen species in Zucker diabetic fatty (ZDF) obese rats were higher than those in ZDF lean rats. Hydrogen peroxide (H(2)O(2)) induced an increase in the AGT expression in primary rat mesangial cells. Furthermore, the H(2)O(2)-induced upregulation of AGT was inhibited by a mitogen-activated protein kinase kinase and a c-Jun N-terminal kinase inhibitor. These data suggest the potential contribution of enhanced AGT expression in glomeruli to the intrarenal RAS activation for the development of glomerular disease.
Authors:
Maki Urushihara; Hiroyuki Kobori
Publication Detail:
Type:  JOURNAL ARTICLE    
Journal Detail:
Title:  International journal of clinical medicine     Volume:  2     ISSN:  2158-2882     ISO Abbreviation:  Int J Clin Med     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2012-1-16     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101571689     Medline TA:  Int J Clin Med     Country:  -    
Other Details:
Languages:  ENG     Pagination:  378-387     Citation Subset:  -    
Affiliation:
Department of Physiology, and Hypertension and Renal Center of Excellence Tulane University Health Sciences Center, New Orleans, USA.
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Descriptor/Qualifier:
Grant Support
ID/Acronym/Agency:
R01 DK072408-01A1//NIDDK NIH HHS

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