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Table of Contents
Vol. 96, No. 1, 2004
Issue release date: January 2004
Section title: Original Paper
Nephron Physiol 2004;96:p1–p10
(DOI:10.1159/000075574)

Regulation of Plasma Hemopexin Activity by Stimulated Endothelial or Mesangial Cells

Kapojos J.J.a · Poelstra K.b · Borghuis T.a · Banas B.c · Bakker W.W.a
Departments of aPathology and Laboratory Medicine, and bPharmacokinetics and Drug Delivery, University of Groningen, Groningen, The Netherlands; cNephrological Center, Medical Policlinic, Ludwig-Maximilians University, Munich, Germany

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: February 02, 2004
Issue release date: January 2004

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

ISSN: (Print)
eISSN: 1660-2137 (Online)

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

Abstract

The pathogenesis of glomerular alterations and proteinuria in corticosteroid-responsive nephrotic syndrome (CRNS) is unknown. As an isoform of plasma hemopexin (Hx) with protease activity may be implicated in this disease, we have studied the inhibition of Hx by ADP and reactivation to its active form by endothelial or mesangial cells in vitro. We hypothesized that these cells might potentially be able to convert the inactivated form of Hx (Hxi) to active Hx (Hxa) in vitro, mediated by cellular ecto-ADPase. Since ecto-ADPase (CD39) is upregulated after stimulation of these cells with lipopolysaccharide (LPS) or certain cytokines, we postulated that this conversion might occur specifically after inflammatory stimulation of these cells. Human endothelial or mesangial cell cultures were incubated overnight with or without LPS (10.0 ng/ml) or TNFα (10.0 ng/ml), washed and subsequently incubated with Hxi (1.5 mg/ml) in serum-free conditions (Hxi was prepared by treatment of Hxa with ADP or ADP-β-S). After 60 min, supernatants were tested for their capacity to alter glomerular extracellular matrix molecules (i.e. ecto-apyrase) in vitro using standard methods, and compared with Hxi that had not been incubated with cells. Supernatants containing Hxa (1.5 mg/ml) served as positive control. The results show significant activity in supernatants with Hxi (prepared using native ADP). However, Hxi inactivated by ADP-β-S (which is non-hydrolyzable) could not be reactivated after contact with LPS-stimulated or unstimulated cells in vitro. As ecto-ADPase of these cells is upregulated by LPS, we believe that reactivation of Hxi to Hxa is mediated by cellular ecto-ADPase. Although the relevance of this inflammation-mediated activation mechanism of Hx in patients with CRNS requires further experimentation, our preliminary observations suggesting that this mechanism is corticosteroid dependent may support a potential role of Hxa in CRNS.

© 2004 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: February 02, 2004
Issue release date: January 2004

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

ISSN: (Print)
eISSN: 1660-2137 (Online)

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


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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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