Age-dependent posttranslational modifications of voltage-dependent anion channel 1

The accumulation of oxidative damage in mitochondrial proteins, membranes and DNA during ageing is supposed to lead to mitochondrial inactivation, downstream molecular impairments and subsequent decline of biological systems. In a quantitative study investigating the age-related changes of mitochond...

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Bibliographic Details
Published in:Experimental gerontology 2010-08, Vol.45 (7-8), p.632-637
Main Authors: Groebe, Karlfried, Klemm-Manns, Martina, Schwall, Gerhard P., Hübenthal, Heiko, Unterluggauer, Herrmann, Jansen-Dürr, Pidder, Tanguay, Robert M., Morrow, Geneviève, Schrattenholz, André
Format: Article
Language:English
Subjects:
Ageing model
Aging - metabolism
Animals
Animals, Genetically Modified
Cells, Cultured
Cellular Senescence - physiology
Drosophila
Drosophila melanogaster - genetics
Drosophila melanogaster - metabolism
Drosophila Proteins - genetics
Drosophila Proteins - metabolism
Embryonic Stem Cells - cytology
Embryonic Stem Cells - metabolism
Endothelial Cells - metabolism
Heat-Shock Proteins - genetics
Heat-Shock Proteins - metabolism
HSP 22
Humans
In Vitro Techniques
Longevity
Male
Mice
Mitochondria - metabolism
Mitochondrial apoptosis
Mitochondrial permeability transition pore
Mutation
Neurons - cytology
Neurons - metabolism
Oxidative posttranslational modifications
PARP-1
Protein Processing, Post-Translational
Proteomics
Quantitative proteomics
Systems biology
Voltage-dependent anion channel 1
Voltage-Dependent Anion Channel 1 - metabolism
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Summary:The accumulation of oxidative damage in mitochondrial proteins, membranes and DNA during ageing is supposed to lead to mitochondrial inactivation, downstream molecular impairments and subsequent decline of biological systems. In a quantitative study investigating the age-related changes of mitochondrial proteins on the level of oxidative posttranslational modifications, we previously found a set of conserved biomarkers across ageing models in five species with consistent oxidative break-up of tryptophan residues and formation of N-formyl kynurenine. In an additional proteomic profiling of a long-living Drosophila mutant overexpressing mitochondrial Hsp22 and controls, we found age-related redundant isoforms of voltage-dependent anion channel 1 (VDAC-1). A re-examination of data from human umbilical vein endothelial cells (with normal and chemically accelerated in vitro ageing), revealed similar age-dependent alterations of voltage-dependent anion channel isoforms. Building on these results, we examined the expression of VDAC-1 in an in vitro model of excitotoxicity. We show that glutamate-induced calcium toxicity in neurons induces changes of voltage-dependent anion channel 1 related to downstream events of mitochondrial apoptosis like poly-ADP-ribosylation.
ISSN:0531-5565
1873-6815
DOI:10.1016/j.exger.2010.02.006