Document Detail


Tubular overexpression of transforming growth factor-beta1 induces autophagy and fibrosis but not mesenchymal transition of renal epithelial cells.
MedLine Citation:
PMID:  20616344     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We recently showed in a tetracycline-controlled transgenic mouse model that overexpression of transforming growth factor (TGF)-beta1 in renal tubules induces widespread peritubular fibrosis and focal degeneration of nephrons. In the present study we have analyzed the mechanisms underlying these phenomena. The initial response to tubular cell-derived TGF-beta1 consisted of a robust proliferation of peritubular cells and deposition of collagen. On sustained expression, nephrons degenerated in a focal pattern. This process started with tubular dedifferentiation and proceeded to total decomposition of tubular cells by autophagy. The final outcome was empty collapsed remnants of tubular basement membrane embedded into a dense collagenous fibrous tissue. The corresponding glomeruli survived as atubular remnants. Thus, TGF-beta1 driven autophagy may represent a novel mechanism of tubular decomposition. The fibrosis seen in between intact tubules and in areas of tubular decomposition resulted from myofibroblasts that were derived from local fibroblasts. No evidence was found for a transition of tubular cells into myofibroblasts. Neither tracing of injured tubules in electron micrographs nor genetic tagging of tubular epithelial cells revealed cells transgressing the tubular basement membrane. In conclusion, overexpression of TGF-beta1 in renal tubules in vivo induces interstitial proliferation, tubular autophagy, and fibrosis, but not epithelial-to-mesenchymal transition.
Authors:
Robert Koesters; Brigitte Kaissling; Michel Lehir; Nicolas Picard; Franziska Theilig; Rolf Gebhardt; Adam B Glick; Brunhilde Hähnel; Hiltraud Hosser; Hermann-Josef Gröne; Wilhelm Kriz
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-07-08
Journal Detail:
Title:  The American journal of pathology     Volume:  177     ISSN:  1525-2191     ISO Abbreviation:  Am. J. Pathol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-08-03     Completed Date:  2011-01-25     Revised Date:  2011-08-03    
Medline Journal Info:
Nlm Unique ID:  0370502     Medline TA:  Am J Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  632-43     Citation Subset:  AIM; IM    
Affiliation:
Institute of Human Genetics, University of Heidelberg, Heidelberg, Germany.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autophagy / physiology*
Epithelial Cells / physiology*,  ultrastructure
Epithelial-Mesenchymal Transition / physiology*
Fibrosis / metabolism,  pathology
Kidney* / cytology,  metabolism,  pathology
Kidney Tubules* / metabolism,  ultrastructure
Mice
Mice, Inbred Strains
Mice, Transgenic
Transforming Growth Factor beta1 / metabolism*
Chemical
Reg. No./Substance:
0/Transforming Growth Factor beta1
Comments/Corrections

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