The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Bcl-2 prevents apoptotic mitochondrial dysfunction by regulating proton flux
Open accessAbstract
We and others have recently shown that loss of the mitochondrial membrane potential (Δψ) precedes apoptosis and chemical-hypoxia-induced necrosis and is prevented by Bcl-2. In this report, we examine the biochemical mechanism used by Bcl-2 to prevent Δψ loss, as determined with mitochondria isolated from a cell line overexpressing human Bcl-2 or from livers of Bcl-2 transgenic mice. Although Bcl-2 had no effect on the respiration rate of isolated mitochondria, it prevented both Δψ loss and the permeability transition (PT) induced by various reagents, including Ca 2+ , H 2 O 2 , and tert -butyl hydroperoxide. Even under conditions that did not allow PT, Bcl-2 maintained Δψ, suggesting that the functional target of Bcl-2 is regulation of Δψ but not PT. Bcl-2 also maintained Δψ in the presence of the protonophore SF6847, which induces proton influx, suggesting that Bcl-2 regulates ion transport to maintain Δψ. Although treatment with SF6847 in the absence of Ca 2+ caused massive H + influx in control mitochondria, the presence of Bcl-2 induced H + efflux after transient H + influx. In this case, Bcl-2 did not enhance K + efflux. Furthermore, Bcl-2 enhanced H + efflux but not K + flux after treatment of mitochondria with Ca 2+ or tert -butyl hydroperoxide. These results suggest that Bcl-2 maintains Δψ by enhancing H + efflux in the presence of Δψ-loss-inducing stimuli.
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Cites
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Self-citationBid acts on the permeability transition pore complex to induce apoptosis
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Metadata
- Authors
- Shimizu, S., Eguchi, Y., Kamiike, W., Funahashi, Y., Mignon, A., Lacronique, V., Matsuda, H., & Tsujimoto, Y.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1998-02-17
- Volume
- 95
- Issue
- 4
- Pages
- 1455-1459
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2168496647
- Cited by
- 410
- References
- 1
- FWCI
- 14.74
- Type
- journal article
- Language
- en
- Open access
- green
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