ArticleBMC medical genetics2009
Voltage-dependent anion channel (VDAC) is involved in apoptosis of cell lines carrying the mitochondrial DNA mutation.
Article in BMC medical genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Calcium Ions Aggravate Alzheimer's Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits.Frontiers in molecular neuroscience · 2021Review
- Protective Effect of Mitochondrial ND2 C5178A Gene Mutation on Cell and Mitochondrial Functions.Oxidative medicine and cellular longevity · 2021Article
- Contribution of Mitochondrial DNA Variation to Chronic Disease in East Asian Populations.Frontiers in molecular biosciences · 2019Review
- Mitochondrial biogenesis dysfunction and metabolic dysfunction from a novel mitochondrial tRNAScientific reports · 2017Article
- Mitochondrial Dynamics and Heart Failure.Comprehensive Physiology · 2015Review
- Proteomic analysis and functional characterization of mouse brain mitochondria during aging reveal alterations in energy metabolism.Proteomics · 2015Article
- The association of receptor of activated protein kinase C 1(RACK1) with infectious bursal disease virus viral protein VP5 and voltage-dependent anion channel 2 (VDAC2) inhibits apoptosis and enhances viral replication.The Journal of biological chemistry · 2015Article
- Quantitative proteomics of synaptic and nonsynaptic mitochondria: insights for synaptic mitochondrial vulnerability.Journal of proteome research · 2014Article
- Aging synaptic mitochondria exhibit dynamic proteomic changes while maintaining bioenergetic function.Aging · 2014Article
- PTB-associated splicing factor (PSF) is a PPARγ-binding protein and growth regulator of colon cancer cells.PloS one · 2013Article
- Critical role for voltage-dependent anion channel 2 in infectious bursal disease virus-induced apoptosis in host cells via interaction with VP5.Journal of virology · 2012Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe mitochondrial voltage-dependent anion channel (VDAC) is increasingly implicated in the control of apoptosis. We have studied the effects the mitochondrial DNA (mtDNA) tRNAIle mutation on VDAC expression, localization, and apoptosis.
methodsLymphoblastoid cell lines were derived from 3 symptomatic and 1 asymptomatic members of a family with hypertension associated with the A4263G tRNAIle mutation as well as from control subjects. Mitochondrial potential (DeltaPsim) and apoptosis were measured by flow cytometry; co-localization of VDAC and Bax was evaluated by confocal microscopy.
resultsExpression of VDAC and Bax in mtDNA cell lines was found to be increased compared to controls, while expression of the small conductance calcium-dependant potassium channel (sKCa) was unchanged. Confocal imaging revealed co-localization of VDAC/Bax on the outer mitochondrial membrane of A4263G cell lines but not from controls. Flow cytometry indicated that the mitochondrial potential was decreased by 32% in mutated cells versus controls while rates of apoptosis were increased (P < 0.05). The difference was attenuated by Cyclosporin A (CsA, 2 muM), a blocker of VDAC.
conclusionWe conclude that increased expression of mitochondrial VDAC and subcellular co-localization of VDAC/Bax increases mitochondrial permeability and apoptosis in cell lines carrying the mtDNA tRNAIle A4263G mutation.
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