Journal of the American Society of Nephrology
2007 JASN IMPACT FACTOR 7.111 HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP 
    advanced
CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Essig, M.
Right arrow Articles by Friedlander, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Essig, M.
Right arrow Articles by Friedlander, G.
J Am Soc Nephrol 14:S33-S35, 2003
© 2003 American Society of Nephrology

Tubular Shear Stress and Phenotype of Renal Proximal Tubular Cells

Marie Essig and Gérard Friedlander

INSERM U 426 and Department of Physiology, Faculté de Médecine Xavier Bichat, Université Denis Diderot–Paris 7, Paris, France.

Correspondence to Marie Essig, Inserm U 426, Faculté de Médecine Xavier Bichat, 16, rue Henri Huchard, F-75018, Paris, France; Phone: 33-1-44-85-62-70; Fax: 33-1-42-28-15-64;

ABSTRACT. Phenotypic alterations resulting from flow-induced mechanical strains is a growing field of research in many cell types such as vascular endothelial and smooth muscle cells, chondrocytes, and osteocytes. Because renal mass reduction is followed by a dramatic increase in GFR in the remaining nephron, modulation of tubular cell phenotype by flow-induced mechanical strains could be one of the events initiating the deleterious pathways that lead to the destruction of renal parenchyma after renal mass reduction. This study demonstrates that increased flow induced, in vitro and in vivo, a reinforcement of the apical domain of actin cytoskeleton and an inhibition of plasminogen activator expression. These effects of flow on plasminogen activator expression were prevented by blocking the reorganization of actin cytoskeleton and were associated with an increase in a shear-stress responsive element binding activity. These results confirm that tubular flow affects the phenotype of renal epithelial cells and suggest that flow-induced mechanical strains could be one determinant of tubulointerstitial lesions during the progression of renal diseases. E-mail: essig@bichat.inserm.fr






HOME CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION AUTHOR INFO
EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673