Document Detail


TRB3 is stimulated in diabetic kidneys, regulated by the ER stress marker CHOP, and is a suppressor of podocyte MCP-1.
MedLine Citation:
PMID:  20660016     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The prevalence of diabetic nephropathy continues to rise, highlighting the importance of investigating and discovering novel treatment strategies. TRB3 is a kinase-like molecule that modifies cellular survival and metabolism and interferes with signal transduction pathways. Herein, we report that TRB3 expression is increased in the kidneys of type 1 and type 2 diabetic mice. TRB3 is expressed in conditionally immortalized podocytes; however, it is not stimulated by elevated glucose. The diabetic milieu is associated with increased oxidative stress and circulating free fatty acids (FFA). We show that reactive oxygen species (ROS) such as H(2)O(2) and superoxide anion (via the xanthine/xanthine oxidase reaction) as well as the FFA palmitate augment TRB3 expression in podocytes. C/EBP homologous protein (CHOP) is a transcription factor that is associated with the endoplasmic reticulum stress response. CHOP expression increases in diabetic mouse kidneys and in podocytes treated with ROS and FFA. In podocytes, transfection of CHOP increases TRB3 expression, and ROS augment recruitment of CHOP to the proximal TRB3 promoter. MCP-1/CCL2 is a chemokine that contributes to the inflammatory injury associated with diabetic nephropathy. In these studies, we demonstrate that TRB3 can inhibit basal and stimulated podocyte production of MCP-1. In summary, enhanced ROS and/or FFA associated with the diabetic milieu induce podocyte CHOP and TRB3 expression. Because TRB3 inhibits MCP-1, manipulation of TRB3 expression could provide a novel therapeutic approach in diabetic kidney disease.
Authors:
Elizabeth Morse; Jana Schroth; Young-Hyun You; Donald P Pizzo; Shinichi Okada; Satish Ramachandrarao; Volker Vallon; Kumar Sharma; Robyn Cunard
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Publication Detail:
Type:  Editorial; Research Support, N.I.H., Extramural     Date:  2010-07-21
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  299     ISSN:  1522-1466     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-04     Completed Date:  2010-12-02     Revised Date:  2011-11-01    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F965-72     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western
Cell Cycle Proteins / biosynthesis*,  genetics,  pharmacology
Chemokine CCL2 / antagonists & inhibitors*,  biosynthesis
Chromatin / metabolism
DNA / biosynthesis,  genetics
Diabetes Mellitus, Experimental / metabolism
Diabetic Nephropathies / metabolism*
Endoplasmic Reticulum / metabolism*
Fluorescent Antibody Technique
Immunoprecipitation
Kidney / cytology,  metabolism
Male
Mice
Mice, Inbred C57BL
Palmitates / metabolism
Plasmids / genetics
Podocytes / metabolism*
RNA, Messenger / biosynthesis,  genetics
Reactive Oxygen Species / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Transcription Factor CHOP / metabolism*
Up-Regulation / drug effects
Grant Support
ID/Acronym/Agency:
P30-DK-063491/DK/NIDDK NIH HHS; R01-DK-56248/DK/NIDDK NIH HHS; U01-DK-076133-02/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Ccl2 protein, mouse; 0/Cell Cycle Proteins; 0/Chemokine CCL2; 0/Chromatin; 0/Palmitates; 0/RNA, Messenger; 0/Reactive Oxygen Species; 0/TRB3 protein, mouse; 147336-12-7/Transcription Factor CHOP; 9007-49-2/DNA
Comments/Corrections
Comment In:
Am J Physiol Renal Physiol. 2010 Nov;299(5):F963-4   [PMID:  20739396 ]

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