Bcl-X-L inhibits Bax-induced alterations in mitochondrial respiration and calcium release

Bcl-X-L inhibits Bax-induced alterations in mitochondrial respiration and calcium release

Author Teles, A. V. F. Autor UNIFESP Google Scholar
Ureshino, R. P. Autor UNIFESP Google Scholar
Dorta, D. J. Autor UNIFESP Google Scholar
Lopes, G. S. Autor UNIFESP Google Scholar
Hsu, Y. -T. Google Scholar
Smaili, Soraya Soubhi Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Med Univ S Carolina
Abstract Apoptosis is a natural cell elimination process involved in a number of physiological and pathological events. This process can be regulated by members of the Bcl-2 family. Bax, a pro-apoptotic member of this family, accelerates cell death, while the pro-survival member, Bcl-X-L, can antagonize the pro-apoptotic function of Bax to promote cell survival. in the present study, we have evaluated the effect of Bcl-X-L on Bax-induced alterations in mitochondrial. respiration and calcium release. We found that in primary cultured astrocytes, recombinant Bcl-X-L is able to antagonize Bax-induced decrease in mitochondrial respiration and increase in mitochondrial. calcium release. in addition, we found that Bcl-X-L can lower the calcium store in the endoplasmic reticulum, thus limiting potential calcium flux induced by apoptosis. This regulation of calcium flux by Bcl-X-L may represent an important mechanism by which this protein promotes cell survival. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
Keywords Bcl-X-L
Bax
calcium
apoptosis
mitochondria
respiratory chain
ATP
ADP
cell death
Language English
Sponsor NIH
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Grant number NIH: NS40932
Date 2008-09-12
Published in Neuroscience Letters. Clare: Elsevier B.V., v. 442, n. 2, p. 96-99, 2008.
ISSN 0304-3940 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 96-99
Origin http://dx.doi.org/10.1016/j.neulet.2008.06.073
Access rights Closed access
Type Article
Web of Science ID WOS:000258909500004
URI http://repositorio.unifesp.br/handle/11600/30904

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