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

Autor 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, S. S. Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Med Univ S Carolina
Resumo 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.
Palavra-chave Bcl-X-L
Bax
calcium
apoptosis
mitochondria
respiratory chain
ATP
ADP
cell death
Idioma Inglês
Financiador NIH
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Número do financiamento NIH: NS40932
Data de publicação 2008-09-12
Publicado em Neuroscience Letters. Clare: Elsevier B.V., v. 442, n. 2, p. 96-99, 2008.
ISSN 0304-3940 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 96-99
Fonte http://dx.doi.org/10.1016/j.neulet.2008.06.073
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000258909500004
Endereço permanente http://repositorio.unifesp.br/handle/11600/30904

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