Document Detail


Mechanical forces and TGFbeta1 reduce podocyte adhesion through alpha3beta1 integrin downregulation.
MedLine Citation:
PMID:  19420102     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Podocyturia is a marker of diabetic nephr- opathy, a possible determinant of its progression and a powerful risk factor for cardiovascular disease. A reduction in podocyte adhesion to the glomerular basement membrane (GBM) via downregulation of alpha3beta1 integrin expression, the main podocyte anchoring dimer to the GBM, may represent one of the mechanisms of podocyturia in glomerular disease. This study investigated the role of mechanical forces and transforming growth factor beta1 (TGFbeta1) in podocyte adhesion and integrin expression. METHODS: Conditionally immortalized murine podocytes were exposed to mechanical stretch and/or TGFbeta1 for 48 h. Podocyte adhesion, apoptosis and alpha3beta1 integrin expression were assessed. RESULTS: Stretch and TGFbeta1 significantly reduced podocyte adhesion and alpha3beta1 integrin expression, events paralleled by increased apoptosis. Blockade of beta1 integrin, with a specific antibody, demonstrated a reduced podocyte adhesion indicating that beta1 integrin downregulation was required for the loss of podocyte adhesion. This was linked to an increase in podocyte apoptosis. The role of apoptosis in podocyte adhesion was further investigated using caspase-3 inhibitors. Podocyte apoptosis inhibition did not affect stretch- and TGFbeta1-mediated integrin downregulation and the loss of podocyte adhesion, suggesting that alpha3beta1 integrin downregulation is sufficient to alter cell adhesion. Although stretch significantly increased podocyte TGFbeta type I, II and III receptors but not podocyte TGFbeta1 secretion, the combination of stretch and TGFbeta1 did not show any additive or synergistic effects on podocyte adhesion and alpha3beta1 integrin expression. CONCLUSIONS: These results suggest that downregulation of alpha3beta1 integrin expression, by mechanical forces or TGFbeta1, is per se sufficient to reduce podocyte adhesion. Apoptosis may represent a parallel important determinant of the podocyte loss from the GBM.
Authors:
Cecile Dessapt; Marc Olivier Baradez; Anthea Hayward; Alessandra Dei Cas; Stephen M Thomas; Giancarlo Viberti; Luigi Gnudi
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-05-06
Journal Detail:
Title:  Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association     Volume:  24     ISSN:  1460-2385     ISO Abbreviation:  Nephrol. Dial. Transplant.     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-08-18     Completed Date:  2009-12-01     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8706402     Medline TA:  Nephrol Dial Transplant     Country:  England    
Other Details:
Languages:  eng     Pagination:  2645-55     Citation Subset:  IM    
Affiliation:
King's College London, UK.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects,  physiology
Cell Adhesion / drug effects,  physiology
Cells, Cultured
Down-Regulation / drug effects
Extracellular Matrix / physiology
Glomerular Basement Membrane / cytology,  drug effects,  physiology
Glycosylation
Integrin alpha3beta1 / chemistry,  physiology*
Kidney Diseases / etiology,  pathology,  physiopathology
Mice
Podocytes / cytology,  drug effects*,  physiology*
Receptors, Transforming Growth Factor beta / classification,  physiology
Stress, Mechanical
Transforming Growth Factor beta1 / pharmacology*
Chemical
Reg. No./Substance:
0/Integrin alpha3beta1; 0/Receptors, Transforming Growth Factor beta; 0/Transforming Growth Factor beta1

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


Previous Document:  Greater loss of axons in primary progressive multiple sclerosis plaques compared to secondary progre...
Next Document:  Optimization of mid-dilution haemodiafiltration: technique and performance.