Document Detail


Retinoids augment the expression of podocyte proteins by glomerular parietal epithelial cells in experimental glomerular disease.
MedLine Citation:
PMID:  23107969     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND/AIMS: A decrease in glomerular podocyte number in membranous nephropathy and focal segmental glomerulosclerosis (FSGS) ultimately underlines glomerulosclerosis and the decrease in kidney function. Recent studies have shown that in these diseases, glomerular parietal epithelial cells begin to express proteins considered unique to podocytes, and that these glomerular epithelial transition cells might serve as podocyte progenitors. Because retinoids improve many forms of experimental glomerular disease characterized by podocyte injury and loss, we asked if all-trans retinoic acid (ATRA) induces parietal epithelial cells to express podocyte proteins.
METHODS: ATRA or vehicle was administered to rats with experimental membranous nephropathy (passive Heymann nephritis model) and mice with experimental FSGS (anti-glomerular antibody model) following the onset of proteinuria. Immunohistochemistry staining of PAX2 (parietal epithelial cell marker), WT-1 (podocyte cell marker), and Ki-67 (proliferation marker) were performed on kidney tissues.
RESULTS: Compared to diseased animals receiving vehicle, ATRA statistically significantly increased the number of glomerular transition cells, defined as cells double-staining for PAX2 and WT-1, in membranous nephropathy at weeks 2, 5 and 16, and in FSGS at weeks 1 and 2. This was accompanied by an increase in the number of podocytes compared to diseased controls receiving vehicle.
CONCLUSION: ATRA increases the number of glomerular epithelial transition cells in experimental proteinuric glomerular diseases. Thus, ATRA may provide a useful pharmacologic approach to decipher the mechanisms underlying the possible progenitor role of parietal epithelial cells.
Authors:
Jiong Zhang; Jeffrey W Pippin; Michael R Vaughan; Ronald D Krofft; Yoshinori Taniguchi; Paola Romagnani; Peter J Nelson; Zhi-Hong Liu; Stuart J Shankland
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-10-25
Journal Detail:
Title:  Nephron. Experimental nephrology     Volume:  121     ISSN:  1660-2129     ISO Abbreviation:  Nephron Exp. Nephrol.     Publication Date:  2012  
Date Detail:
Created Date:  2012-12-21     Completed Date:  2013-07-09     Revised Date:  2014-04-07    
Medline Journal Info:
Nlm Unique ID:  101159770     Medline TA:  Nephron Exp Nephrol     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  e23-37     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 S. Karger AG, Basel.
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MeSH Terms
Descriptor/Qualifier:
Animals
Glomerulonephritis, Membranous / drug therapy*,  metabolism*,  pathology
Ki-67 Antigen / metabolism*
Male
Mice
PAX2 Transcription Factor / metabolism*
Podocytes / drug effects,  metabolism*
Rats
Rats, Sprague-Dawley
Treatment Outcome
Tretinoin / administration & dosage*
Up-Regulation / drug effects
WT1 Proteins / metabolism*
Grant Support
ID/Acronym/Agency:
R01 DK056799/DK/NIDDK NIH HHS; R01DK056799/DK/NIDDK NIH HHS; R21 DK081835/DK/NIDDK NIH HHS; R21DK081835/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Ki-67 Antigen; 0/PAX2 Transcription Factor; 0/PAX2 protein, rat; 0/WT1 Proteins; 5688UTC01R/Tretinoin
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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