Bax affects intracellular Ca2+ stores and induces Ca2+ wave propagation

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2004-12-01
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Carvalho, ACP
Sharpe, J.
Rosenstock, T. R.
Teles, AFV
Youle, R. J.
Smaili, Soraya Soubhi [UNIFESP]
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In the present study, we evaluated proapoptotic protein Bax on mitochondria and Ca2+ homeostasis in primary cultured astrocytes. We found that recombinant Bax (rBax, 10 and 100 ng/ml) induces a loss in mitochondrial membrane potential (DeltaPsi(m)). This effect might be related to the inhibition of respiratory rates and a partial release of cytochrome c, which may change mitochondrial morphology. the loss of DeltaPsi(m) and a selective permeabilization of mitochondrial membranes contribute to the release of Ca2+ from the mitochondria. This was inhibited by cyclosporin A (5 muM) and Ruthenium Red (1 mug/ml), indicating the involvement of mitochondrial Ca2+ transport mechanisms. Bax-induced mitochondrial Ca2+ release evokes Ca2+ waves and wave propagation between cells. Our results show that Bax induces mitochondrial alteration that affects Ca2+ homeostasis and signaling. These changes show that Ca2+ signals might be correlated with the proapoptotic activities of Bax.
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Cell Death and Differentiation. London: Nature Publishing Group, v. 11, n. 12, p. 1265-1276, 2004.
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