The DOI matches its Crossref record; 71 of the 71 references it cites were found in a registry or an index.
Outer membrane VDAC1 controls permeability transition of the inner mitochondrial membrane in cellulo during stress-induced apoptosis
Abstract
Voltage-dependent anion channel (VDAC)1 is the main channel of the mitochondrial outer membrane (MOM) and it has been proposed to be part of the permeability transition pore (PTP), a putative multiprotein complex candidate agent of the mitochondrial permeability transition (MPT). Working at the single live cell level, we found that overexpression of VDAC1 triggers MPT at the mitochondrial inner membrane (MIM). Conversely, silencing VDAC1 expression results in the inhibition of MPT caused by selenite-induced oxidative stress. This MOM-MIM crosstalk was modulated by Cyclosporin A and mitochondrial Cyclophilin D, but not by Bcl-2 and Bcl-X(L), indicative of PTP operation. VDAC1-dependent MPT engages a positive feedback loop involving reactive oxygen species and p38-MAPK, and secondarily triggers a canonical apoptotic response including Bax activation, cytochrome c release and caspase 3 activation. Our data thus support a model of the PTP complex involving VDAC1 at the MOM, and indicate that VDAC1-dependent MPT is an upstream mechanism playing a causal role in oxidative stress-induced apoptosis.
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“In particular, the outer membrane transporter VDAC has been shown, by several studies, to control mPTP activity [6,22,23,24,25,26,27].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [22]
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Cites
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Metadata
- Authors
- Tomasello, F., Messina, A., Lartigue, L., Schembri, L., Medina, C., Reina, S., Thoraval, D., Crouzet, M., Ichas, F., De Pinto, V., & De Giorgi, F.
- Affiliations
- University of Catania (IT)
- Inserm (FR)
- Centre National de la Recherche Scientifique (FR)
- Venue
- Cell Research
- Published
- 2009-08-11
- Volume
- 19
- Issue
- 12
- Pages
- 1363-1376
- ISSN
- 1001-0602 (ISSN-L)
- 1748-7838
- OpenAlex
- W2054828537
- Cited by
- 161
- References
- 71
- Citations by year
- 2026: 11 · 2025: 13 · 2024: 7 · 2023: 5 · 2022: 4 · 2021: 8 · 2020: 13 · 2019: 7 · 2018: 7 · 2017: 12 · 2016: 11 · 2015: 11 · 2014: 14 · 2013: 8 · 2012: 8
- FWCI
- 4.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Research (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Institut National de la Santé et de la Recherche Médicale
- Ligue Contre le Cancer
- Università di Catania
- Institut Bergonié
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- VDAC1, mitochondrial permeability transition, mitochondrial permeability transition pore, mitochondrial outer membrane, inner mitochondrial membrane, oxidative stress-induced apoptosis, selenite, cyclosporine, cyclophilin D, reactive oxygen species, p38 MAPK, Bax activation, cytochrome c release, caspase-3
- MeSH terms
- Peptidyl-Prolyl Isomerase F, Animals, Cell Membrane Permeability, Chlorocebus aethiops, HeLa Cells, Humans, Stress, Physiological, Cyclosporine, Sodium Selenite, Oxidative Stress, COS Cells, Gene Silencing, Cyclophilins, Feedback, Physiological, Voltage-Dependent Anion Channel 1, Apoptosis Regulatory Proteins, Mitochondrial Membranes, Membrane Potential, Mitochondrial
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