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Vol. 29, No. 6, 2009
Issue release date: June 2009
Section title: Original Report: Laboratory Investigation
Am J Nephrol 2009;29:538–550
(DOI:10.1159/000191467)

Angiotensin II Upregulates RAGE Expression on Podocytes: Role of AT2 Receptors

Rüster C. · Bondeva T. · Franke S. · Tanaka N. · Yamamoto H. · Wolf G.
aKlinik für Innere Medizin III, Friedrich Schiller University, Jena, Germany; bDepartment of Biochemistry and Molecular Vascular Biology, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, and cDepartment of Ophthalmology, Kyorin University School of Medicine, Kyorin, Japan

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Article / Publication Details

First-Page Preview
Abstract of Original Report: Laboratory Investigation

Received: 9/3/2008
Accepted: 11/19/2008
Published online: 1/8/2009

Number of Print Pages: 13
Number of Figures: 10
Number of Tables: 0

ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)

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

Abstract

Background: Advanced glycation end products (AGEs) play an important role in diabetic nephropathy. The receptor for AGEs, called RAGE, is present on podocytes. We investigated whether angiotensin II (ANG II) modulates RAGE expression on cultured differentiated podocytes. Results: Cultured podocytes expressed AT1 and AT2 receptors. Surprisingly, ANG II induced RAGE mRNA and protein expression through AT2 receptors. ANG II had no influence on proliferation or protein content of podocytes. The increase in RAGE expression depended on stimulated transcriptional activity. Using various mutant reporter constructs of the RAGE promoter region, it was shown that a NF-κB binding site at –1519 was essential for ANG II-induced transcriptional activity. Preincubation with ANG II increased the expression of tumor necrosis factor-α mRNA and protein expression induced by AGE, indicating that the ANG II-mediated upregulation of RAGE has functional consequences. AGE-BSA was incorporated into cells as measured by Western blots for Nε-carboxymethyllysine, but ANG II did not influence this process. ANG II in the absence or presence of AGE-BSA did not induce apoptosis of podocytes. Conclusion: Our study revealed aninteraction between the renin-angiotensin system and the AGE/RAGE axis in podocytes. Since intraglomerular ANG II levels are increased in diabetic nephropathy, this interaction may have pathophysiological consequences for podocyte injury and inflammation associated with the development of diabetic nephropathy.


Article / Publication Details

First-Page Preview
Abstract of Original Report: Laboratory Investigation

Received: 9/3/2008
Accepted: 11/19/2008
Published online: 1/8/2009

Number of Print Pages: 13
Number of Figures: 10
Number of Tables: 0

ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)

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


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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 goverment 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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