Voltage-dependent anion channel (VDAC) is involved in apoptosis of cell lines carrying the mitochondrial DNA mutation

The 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.

Methods: Lymphoblastoid cell lines were derived from 3 symptomatic and 1 asymptomatic members of a family with hypertension associated with the A4263G tRNAIle mutationas well as from control subjects.

Mitochondrial potential and apoptosis were measured by flow cytometry; co-localization of VDAC and Bax was evaluated by confocal microscopy.

Results: Expression of VDAC and Bax in mtDNA cell lines was found to be increased compared to controls, while expression of the small conductance calcium-dependantpotassium channel (sKCa) was unchanged. Confocal imaging revealed co-localization of VDAC/Bax on the outer mitochondrial membrane of A4263G cell lines but notfrom controls.

Flow cytometry indicated that the mitochondrial potential was decreased by 32% in mutated cells versus controls while rates of apoptosis wereincreased (P<0.05). The difference was attenuated by Cyclosporin A (CsA, 2 muM), a blocker of VDAC.

Conclusions: We 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.

Author: Liu YuqiLi YangLi ZongbinXu HuaWen YiWang LinGuan MinxinGao LeiWang Shiwen
Credits/Source: BMC Medical Genetics 2009, 10:114

Published on: 2009-11-09

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