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Bax does not directly partecipate in the Ca2+ - induced permeability transition of isolated mitochondria (Articolo in rivista)

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Bax does not directly partecipate in the Ca2+ - induced permeability transition of isolated mitochondria (Articolo in rivista) (literal)

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De Marchi U; Campello S; Szabò I; Tombola F; Martinou JC; Zoratti M (2004)
Bax does not directly partecipate in the Ca2+ - induced permeability transition of isolated mitochondria
in The Journal of biological chemistry (Print)
(literal)

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De Marchi U; Campello S; Tombola F; Zoratti M: IN - Padova e Dip. Scienze Biomediche Sperimentali, Università di Padova. Martinou JC: Dep. of Cell Biology, University of Geneva, Switzerland (literal)

Titolo

Bax does not directly partecipate in the Ca2+ - induced permeability transition of isolated mitochondria (literal)

Abstract

The mitochondrial permeability transition pore and Bax have both been proposed to be involved in the release of pro-apoptotic factors from mitochondria in the \"intrinsic\" pathway of apoptosis. The permeability transition pore is widely thought to be a supramolecular complex including or interacting with Bax. Given the relevance of the permeability transition in vivo, we have verified whether Bax influences the formation and/or the properties of the Ca(2+)/P(i)-induced permeability transition by using mitochondriaisolated from isogenic human colon cancer bax(+/-) and bax(-/-) HCT116 cell lines. We used mitochondria isolated from both types of cells and from Bax(+) cells exposed to apoptotic stimuli, as well as Bax-less mitochondria into which exogenous Bax had been incorporated. All exhibited the same behavior and pharmacological profile in swelling and Ca(2+)-retention experiments. Mitochondria from a bax(-)/bak(-) cell line also underwent an analogous Ca(2+)/P(i)-inducible swelling. This similarity indicates that Bax hasno major role in regulating the Ca(2+)-induced mitochondrial permeability transition. (literal)

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