Skip Navigation



NDT Advance Access published online on July 20, 2004
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfh374
© 2004 by European Renal Association - European Dialysis and Transplant Association
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
19/9/2217    most recent
gfh374v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Vonend, O.
Right arrow Articles by Rump, L. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vonend, O.
Right arrow Articles by Rump, L. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Received September 5, 2003
Accepted May 19, 2004

Original Article

Modulation of gene expression by moxonidine in rats with chronic renal failures

Oliver Vonend 1, Thomas Apel 1, Kerstin Amann 2, Lorenz Sellin 1, Johannes Stegbauer 1, Eberhard Ritz 2, Lars Christian Rump 1*

1 Department of Internal Medicine, Marienhospital Herne, University of Bochum, Germany
2 Department of Pathology, University of Erlangen, Germany

* To whom correspondence should be addressed. E-mail: christian.rump{at}ruhr-uni-bochum.de.



  Abstract

Background. Sympathetic overactivity is a hallmark of chronic renal failure. In a previous experimental study, the sympatholytic drug moxonidine (MOX) had beneficial effects on progression of chronic renal failure. The present study investigates whether moxonidine influences the expression of genes associated with adaptive changes in kidneys of subtotally nephrectomized rats.

Methods. RNA was isolated from remnant kidneys of sham-operated, subtotally nephrectomized (SNX) and moxonidine-treated SNX (SNX-M) rats 12 weeks after operation. Genes that might play a role in renal adaptation processes after subtotal nephrectomy were selected and their expression was analysed by real-time reverse transcription-polymerase chain reaction (RT-PCR).

Results. After subtotal nephrectomy, there was an increase in gene expression of cysteine protease cathepsin (H + L), ATP receptor subtypes P2Y2 and P2Y6, cell cycle regulator p21 and transforming growth factor-{beta}1 (TGF-{beta}1), and a decrease of the metalloprotease aminopeptidase-M (APM), membrane transporter megalin, ageing-related klotho, type I TGF-{beta} receptor, mitochondrial cytochrome oxidase-1, kallikrein, leucine zipper-1, matrix-degrading metalloprotease meprin, the organic anion transporter and the P2 receptor subtypes P2Y1 and P2Y4. In SNX-M rats, mRNA levels of APM, megalin, klotho, TGF-{beta}1, type I TGF-{beta} receptor, p21, P2Y1 and P2Y2 were shifted back towards control levels.

Conclusions. Several genes showing altered expression levels after subtotal nephrectomy were identified in remnant kidneys. These genes might act as candidates to promote disease progression. The sympatholytic drug moxonidine, at a concentration devoid of blood pressure effects, regulates the renal expression of some of these genes back towards control levels. To what extent sympathetic neurotransmitters directly alter expression of these genes in cultured renal cells currently is under investigation.

Keywords: 5/6 nephrectomy; chronic renal failure; gene expression; moxonidine; P2 receptors; sympathetic activity.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Nephrol Dial TransplantHome page
P. Boor, K. Sebekova, T. Ostendorf, and J. Floege
Treatment targets in renal fibrosis
Nephrol. Dial. Transplant., December 1, 2007; 22(12): 3391 - 3407.
[Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.