|
|
Title
|
Up-regulation of Bcl-2 by redox signals in glomerular mesangial cells
|
 |
KB Sandau & B Brüne
Department of Medicine IV-Experimental Division, University of Erlangen-Nürnberg, Faculty of Medicine, 91054 Erlangen, Germany
Correspondence to: B Brüne, University of Erlangen Nürnberg, Faculty of Medicine, Loschgestrasse 8, 91054 Erlangen, Germany. Tel: +49-9131-8536311; Fax: +49-9131-8539202; E-mail: mfm423@rzmail.uni-erlangen.de
Edited by J Stamler
|
Abstract
|
 |
The mediators nitric oxide (NO) and superoxide (O2–) are known to regulate cell death and survival. In mesangial cells (MC), NO induced apoptosis and in higher concentrations necrosis. Intriguingly, cogeneration of NO and O2– in a balanced ratio promoted cell protection. Under these conditions, we noticed the accumulation of the anti-apoptotic protein Bcl-2. Its up-regulation is based on an increase in mRNA and protein level. To investigate whether oxidative stress elicits Bcl-2 expression in general, we further used the chemically unrelated oxidative agents diamide and butyl hydroperoxide. Both stimulated mRNA and protein up-regulation of Bcl-2. But in contrast to diamide, butyl hydroperoxide evoked apoptosis and necrosis despite Bcl-2 accumulation. As diamide was non-toxic, we used diamide as a Bcl-2 activator to protect MC against a subsequent toxic dose of NO. We conclude that redox changes promote Bcl-2 up-regulation that may confer cellular protection towards apoptosis. Cell Death and Differentiation (2000) 7, 118 – 125.
|
 |
Keywords |
 |
Bcl-2; nitric oxide; superoxide; redox signals; apoptosis; protection
|
 |
Received 24 November 1998; Revised 14 September 1999; Accepted 19 October 1999

©
Macmillan Publishers Ltd 2000
|
|
|