Document Detail


PKC-delta promotes renal tubular cell apoptosis associated with proteinuria.
MedLine Citation:
PMID:  20395372     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Proteinuria may contribute to progressive renal damage by inducing tubulointerstitial inflammation, fibrosis, and tubular cell injury and death, but the mechanisms underlying these pathologic changes remain largely unknown. Here, in a rat kidney proximal tubular cell line (RPTC), albumin induced apoptosis in a time- and dose-dependent manner. Caspase activation accompanied albumin-induced apoptosis, and general caspase inhibitors could suppress this activation. In addition, Bcl-2 transfection inhibited apoptosis and attenuated albumin-induced Bax translocation to mitochondria and cytochrome c release from the organelles, further confirming a role for the intrinsic pathway of apoptosis in albuminuria-associated tubular apoptosis. We observed phosphorylation and activation of PKC-delta early during treatment of RPTC cells with albumin. Rottlerin, a pharmacologic inhibitor of PKC-delta, suppressed albumin-induced Bax translocation, cytochrome c release, and apoptosis. Moreover, a dominant-negative mutant of PKC-delta blocked albumin-induced apoptosis in RPTC cells. In vivo, we observed activated PKC-delta in proteinuric kidneys of streptozotocin-induced diabetic mice and in kidneys after direct albumin overload. Notably, albumin overload induced apoptosis in renal tubules, which was less severe in PKC-delta-knockout mice. Taken together, these results suggest that activation of PKC-delta promotes tubular cell injury and death during albuminuria, broadening our understanding of the pathogenesis of progressive proteinuric kidney diseases.
Authors:
Xiaoning Li; Navjotsingh Pabla; Qingqing Wei; Guie Dong; Robert O Messing; Cong-Yi Wang; Zheng Dong
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-04-15
Journal Detail:
Title:  Journal of the American Society of Nephrology : JASN     Volume:  21     ISSN:  1533-3450     ISO Abbreviation:  J. Am. Soc. Nephrol.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-01     Completed Date:  2010-07-21     Revised Date:  2011-08-25    
Medline Journal Info:
Nlm Unique ID:  9013836     Medline TA:  J Am Soc Nephrol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1115-24     Citation Subset:  IM    
Affiliation:
Department of Cellular Biology and Anatomy, Medical College of Georgia and Charlie Norwood Veterans' Affairs Medical Center, Augusta, Georgia 30912, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Acetophenones / pharmacology
Albumins / metabolism,  pharmacology
Animals
Apoptosis / drug effects,  physiology*
Benzopyrans / pharmacology
Caspases / metabolism
Cell Line
Cytochromes c / metabolism
Diabetes Mellitus, Experimental / complications
Disease Models, Animal
Dose-Response Relationship, Drug
Enzyme Inhibitors / pharmacology
Kidney Tubules, Proximal / drug effects,  pathology,  physiopathology*
Male
Mice
Mice, Knockout
Protein Kinase C-delta / antagonists & inhibitors,  genetics,  physiology*
Proteinuria / etiology,  metabolism,  physiopathology*
Proto-Oncogene Proteins c-bcl-2 / metabolism
Rats
Streptozocin
bcl-2-Associated X Protein / metabolism
Chemical
Reg. No./Substance:
0/Acetophenones; 0/Albumins; 0/Benzopyrans; 0/Enzyme Inhibitors; 0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-2-Associated X Protein; 18883-66-4/Streptozocin; 82-08-6/rottlerin; 9007-43-6/Cytochromes c; EC 2.7.11.13/Protein Kinase C-delta; EC 3.4.22.-/Caspases
Comments/Corrections
Comment In:
J Am Soc Nephrol. 2010 Jul;21(7):1063-5   [PMID:  20558537 ]

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


Previous Document:  Dysfunctional endothelial progenitor cells in chronic kidney disease.
Next Document:  Weekend hospital admission, acute kidney injury, and mortality.