Document Detail


Indoxyl sulfate inhibits proliferation of human proximal tubular cells via endoplasmic reticulum stress.
MedLine Citation:
PMID:  20534867     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Uremic toxins can deteriorate renal function, but little is known about its mechanism. Because tubular injury is central to progression of chronic kidney disease (CKD), we investigated the effects of a representative uremic toxin indoxyl sulfate (IS) on tubular cells. IS induced endoplasmic reticulum (ER) stress in cultured human proximal tubular cells, demonstrated by the increase in C/EBP homologous protein (CHOP) in the immunoblots. Moreover, administration of an oral adsorbent AST-120 reduced serum IS concentration and decreased tubular expression of CHOP in immunohistochemistry in 5/6-nephretomized, CKD model, rats. Furthermore, we disclosed that IS inhibited proliferation of tubular cells in 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium and 5-bromo-2'-deoxyuridine assay, whereas the results of trypan blue exclusion and lactate dehydrogenase assay showed that IS did not promote cell death. This inhibition was mitigated by small interfering (si) RNA against CHOP. Furthermore, IS increased the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) (p21). Surprisingly, this was mediated by the inflammatory cytokine interleukin (IL)-6, the expression of which was decreased by siRNA against activating transcription factor 4, another ER stress marker; however, the induction of IL-6 and p21 by IS was not suppressed by siRNA targeted to CHOP, suggesting that they were downstream of ER stress, but independent of CHOP. Moreover, we found that their upregulation was dependent on ERK, using the ERK pathway inhibitor U-0126. Collectively, we demonstrated that IS induced ER stress in tubular cells and inhibited cell proliferation via two pathways downstream of ER stress, namely CHOP and ERK-IL-6-p21. These are possible targets for suppressing progression of CKD.
Authors:
Takahisa Kawakami; Reiko Inagi; Takehiko Wada; Tetsuhiro Tanaka; Toshiro Fujita; Masaomi Nangaku
Related Documents :
15100367 - Local actions of endogenous angiotensin ii in injured glomeruli.
6377897 - Cellular composition of crescents in human rapidly progressive glomerulonephritis ident...
17141057 - Kidney epithelial cells.
17180447 - Human glomerular mesangial ip15 cell line as a suitable model for in vitro cadmium cyto...
2569707 - The ad5 12s growth factor induces f9 cell proliferation and differentiation.
6440787 - Localization of ornithine decarboxylase in mutant cho cells that overproduce the enzyme...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-09
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  299     ISSN:  1522-1466     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-03     Completed Date:  2010-09-24     Revised Date:  2011-04-28    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F568-76     Citation Subset:  IM    
Affiliation:
University of Tokyo School of Medicine, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Carbon / pharmacology
Cell Death / drug effects
Cell Line
Cell Proliferation / drug effects*
Chronic Disease
Cyclin-Dependent Kinase Inhibitor p21 / metabolism
Disease Models, Animal
Endoplasmic Reticulum / drug effects*,  physiology
Extracellular Signal-Regulated MAP Kinases / metabolism
Humans
Indican / pharmacology*
Interleukin-6 / metabolism
Kidney Diseases / metabolism
Kidney Tubules, Proximal / cytology*,  metabolism
Male
Nephrectomy
Oxides / pharmacology
Rats
Rats, Sprague-Dawley
Signal Transduction / physiology
Stress, Physiological / drug effects*,  physiology
Transcription Factor CHOP / metabolism
Chemical
Reg. No./Substance:
0/CDKN1A protein, human; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/DDIT3 protein, human; 0/Ddit3 protein, rat; 0/Interleukin-6; 0/Oxides; 147336-12-7/Transcription Factor CHOP; 487-94-5/Indican; 7440-44-0/Carbon; 90597-58-3/AST 120; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases

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


Previous Document:  Involvement of urinary proteins in the rat strain difference in sensitivity to ethylene glycol-induc...
Next Document:  Phosphate homeostasis and the renal-gastrointestinal axis.