Bcl-2 Modulates Endoplasmic Reticulum and Mitochondrial Calcium Stores in PC12 Cells

Bcl-2 Modulates Endoplasmic Reticulum and Mitochondrial Calcium Stores in PC12 Cells

Autor Hirata, Hanako Autor UNIFESP Google Scholar
Lopes, Guiomar S. Autor UNIFESP Google Scholar
Jurkiewicz, Aron Autor UNIFESP Google Scholar
Garcez-do-Carmo, Lucia Autor UNIFESP Google Scholar
Smaili, Soraya Soubhi Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Resumo Endoplasmic reticulum (ER) and mitochondria are intracellular organelles and their interactions are directly involved in different processes such as Ca2+ signaling in cell survival and death mechanisms. Bcl-2 is an anti-apoptotic protein intrinsically related to ER and mitochondria, modulating Ca2+ content in these organelles. We investigated the effects of Bcl-2 overexpression on ER and mitochondrial Ca2+ dynamics in PC12 cells. Bcl-2 overexpressing and control cells were loaded with Fura 2/AM and stimulated with different drugs. Results showed that in Bcl-2 cells, ACh induced a lower Ca2+ response compared to control. Ca2+ release induced by TG was decreased in Bcl-2 cells, however, it was greater in Caff induced Ca2+ rise. in addition, FCCP induced a higher Ca2+ release in Bcl-2 cells. These results suggest that Bcl-2 overexpression modulate the ER Ca2+ pools differently and the release of ER Ca2+ may increase mitochondrial Ca2+ accumulation. These alterations of intracellular Ca2+ stores are important mechanisms for the control of Ca2+ signaling.
Assunto PC12
Bcl-2
Calcium
ER
Mitochondria
ACh
Idioma Inglês
Financiador Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Data 2012-02-01
Publicado em Neurochemical Research. New York: Springer/plenum Publishers, v. 37, n. 2, p. 238-243, 2012.
ISSN 0364-3190 (Sherpa/Romeo, fator de impacto)
Editor Springer
Extensão 238-243
Fonte http://dx.doi.org/10.1007/s11064-011-0600-5
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000302404100002
URI http://repositorio.unifesp.br/handle/11600/34571

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