Document Detail

Proximal tubular injury and rapid formation of atubular glomeruli in mice with unilateral ureteral obstruction: a new look at an old model.
MedLine Citation:
PMID:  21429968     Owner:  NLM     Status:  MEDLINE    
Unilateral ureteral obstruction (UUO), employed extensively as a model of progressive renal interstitial fibrosis, results in rapid parenchymal deterioration. Atubular glomeruli are formed in many renal disorders, but their identification has been limited by labor-intensive available techniques. The formation of atubular glomeruli was therefore investigated in adult male mice subjected to complete UUO under general anesthesia. In this species, the urinary pole of Bowman's capsule is normally lined by tall parietal epithelial cells similar to those of the proximal tubule, and both avidly bind Lotus tetragonolobus lectin. Following UUO, these cells became flattened, lost their affinity for Lotus lectin, and no longer generated superoxide (revealed by nitroblue tetrazolium infusion). Based on Lotus lectin staining, stereological measurements, and serial section analysis, over 80% of glomeruli underwent marked transformation after 14 days of UUO. The glomerulotubular junction became stenotic and atrophic due to cell death by apoptosis and autophagy, with concomitant remodeling of Bowman's capsule to form atubular glomeruli. In this degenerative process, transformed epithelial cells sealing the urinary pole expressed α-smooth muscle actin, vimentin, and nestin. Although atubular glomeruli remained perfused, renin immunostaining was markedly increased along afferent arterioles, and associated maculae densae disappeared. Numerous progressive kidney disorders, including diabetic nephropathy, are characterized by the formation of atubular glomeruli. The rapidity with which glomerulotubular junctions degenerate, coupled with Lotus lectin as a marker of glomerular integrity, points to new investigative uses for the model of murine UUO focusing on mechanisms of epithelial cell injury and remodeling in addition to fibrogenesis.
Michael S Forbes; Barbara A Thornhill; Robert L Chevalier
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-03-23
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  301     ISSN:  1522-1466     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-07-07     Completed Date:  2011-09-08     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F110-7     Citation Subset:  IM    
Dept. of Pediatrics, University of Virginia, Box 800386, Charlottesville, VA 22908, USA.
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MeSH Terms
Actins / biosynthesis
Acute Kidney Injury / pathology*
Apoptosis / physiology
DNA Fragmentation
Disease Models, Animal
In Situ Nick-End Labeling
Intermediate Filament Proteins / biosynthesis
Kidney Glomerulus / pathology*
Kidney Tubules, Proximal / pathology*
Mice, Inbred C57BL
Nephrons / pathology
Nerve Tissue Proteins / biosynthesis
Oxidative Stress / physiology
Paraffin Embedding
Renin / metabolism
Superoxides / metabolism
Ureteral Obstruction / pathology*
Vimentin / biosynthesis
Grant Support
Reg. No./Substance:
0/Actins; 0/Intermediate Filament Proteins; 0/Lectins; 0/Nerve Tissue Proteins; 0/Vimentin; 0/fucose-binding lectin; 0/nestin; 11062-77-4/Superoxides; EC

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