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Table of Contents
Vol. 116, No. 4, 2010
Issue release date: November 2010
Section title: Original Paper
Nephron Exp Nephrol 2010;116:e72–e83
(DOI:10.1159/000319320)

The Cytoplasmic Domain of Tissue Factor Restricts Physiological Albuminuria and Pathological Proteinuria Associated with Glomerulonephritis in Mice

Apostolopoulos J. · Moussa L. · Tipping P.G.
Centre for Inflammatory Diseases, Department of Medicine, Monash University, Clayton, Vic., Australia

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: December 22, 2009
Accepted: April 16, 2010
Published online: July 28, 2010
Issue release date: November 2010

Number of Print Pages: 1
Number of Figures: 8
Number of Tables: 0

ISSN: (Print)
eISSN: 1660-2129 (Online)

For additional information: http://www.karger.com/NEE

Abstract

Background/Aims: Tissue factor (TF) is a transmembrane protein that is essential for coagulation. TF is expressed on podocytes and its cytoplasmic domain has cell signalling functions in epithelial cells. Methods: Mice lacking the cytoplasmic domain of TF (TFCT–/– mice) were used to study its role in physiological albuminuria and pathological proteinuria following induction of glomerulonephritis (GN). Results: Absence of the cytoplasmic domain of TF was associated with increased albuminuria, podocyte effacement, reduced podocyte numbers and increased spontaneous glomerular tumour necrosis factor α(TNFα) production under physiological conditions. In mice developing GN, absence of the cytoplasmic domain of TF resulted in increased proteinuria and enhanced renal TNFα production without altering other parameters of renal inflammation and injury. Studies in TFCT–/– chimeric mice (created by bone marrow transplantation) showed increased proteinuria and renal TNFα mRNA in GN was associated with absence of the cytoplasmic domain of TF in the kidney and was independent of the leucocyte phenotype. Conclusion: These studies demonstrate that the cytoplasmic domain of TF contributes to renal albumin retention and its renal expression protects against proteinuria in leucocyte-mediated renal inflammation. Increased glomerular production of TNFα in the absence of cytoplasmic domain of TF may contribute to podocyte injury resulting in albuminuria and proteinuria.

© 2010 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: December 22, 2009
Accepted: April 16, 2010
Published online: July 28, 2010
Issue release date: November 2010

Number of Print Pages: 1
Number of Figures: 8
Number of Tables: 0

ISSN: (Print)
eISSN: 1660-2129 (Online)

For additional information: http://www.karger.com/NEE


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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