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Loss of PLA2G6 leads to elevated mitochondrial lipid peroxidation and mitochondrial dysfunction.

Kinghorn KJ, Castillo-Quan JI, Bartolome F, Angelova PR, Li L, Pope S, Cochemé HM, Khan S, Asghari S, Bhatia KP, Hardy J, Abramov AY, Partridge L - Brain (2015)

Bottom Line: Furthermore, we demonstrate that loss of iPLA2-VIA function leads to a number of mitochondrial abnormalities, including mitochondrial respiratory chain dysfunction, reduced ATP synthesis and abnormal mitochondrial morphology.Moreover, we show that loss of iPLA2-VIA is strongly associated with increased lipid peroxidation levels.Similar abnormalities were seen including elevated mitochondrial lipid peroxidation and mitochondrial membrane defects, as well as raised levels of cytoplasmic and mitochondrial reactive oxygen species.

View Article: PubMed Central - PubMed

Affiliation: 1 Institute of Healthy Ageing and Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, UK 2 Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK k.kinghorn@ucl.ac.uk.

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Mutations in PLA2G6, which encodes ‘calcium-independent phospholipase A2 beta’, have been implicated in parkinsonian disorders. Kinghorn et al. show, in a Drosophila model and in human fibroblasts, that reduced PLA2G6 activity is associated with elevated mitochondrial lipid peroxidation and mitochondrial dysfunction. Treatment with deuterated polyunsaturated fatty acids reverses the deficits.
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fig1g: Mutations in PLA2G6, which encodes ‘calcium-independent phospholipase A2 beta’, have been implicated in parkinsonian disorders. Kinghorn et al. show, in a Drosophila model and in human fibroblasts, that reduced PLA2G6 activity is associated with elevated mitochondrial lipid peroxidation and mitochondrial dysfunction. Treatment with deuterated polyunsaturated fatty acids reverses the deficits.


Loss of PLA2G6 leads to elevated mitochondrial lipid peroxidation and mitochondrial dysfunction.

Kinghorn KJ, Castillo-Quan JI, Bartolome F, Angelova PR, Li L, Pope S, Cochemé HM, Khan S, Asghari S, Bhatia KP, Hardy J, Abramov AY, Partridge L - Brain (2015)

Mutations in PLA2G6, which encodes ‘calcium-independent phospholipase A2 beta’, have been implicated in parkinsonian disorders. Kinghorn et al. show, in a Drosophila model and in human fibroblasts, that reduced PLA2G6 activity is associated with elevated mitochondrial lipid peroxidation and mitochondrial dysfunction. Treatment with deuterated polyunsaturated fatty acids reverses the deficits.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4559908&req=5

fig1g: Mutations in PLA2G6, which encodes ‘calcium-independent phospholipase A2 beta’, have been implicated in parkinsonian disorders. Kinghorn et al. show, in a Drosophila model and in human fibroblasts, that reduced PLA2G6 activity is associated with elevated mitochondrial lipid peroxidation and mitochondrial dysfunction. Treatment with deuterated polyunsaturated fatty acids reverses the deficits.
Bottom Line: Furthermore, we demonstrate that loss of iPLA2-VIA function leads to a number of mitochondrial abnormalities, including mitochondrial respiratory chain dysfunction, reduced ATP synthesis and abnormal mitochondrial morphology.Moreover, we show that loss of iPLA2-VIA is strongly associated with increased lipid peroxidation levels.Similar abnormalities were seen including elevated mitochondrial lipid peroxidation and mitochondrial membrane defects, as well as raised levels of cytoplasmic and mitochondrial reactive oxygen species.

View Article: PubMed Central - PubMed

Affiliation: 1 Institute of Healthy Ageing and Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, UK 2 Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK k.kinghorn@ucl.ac.uk.

Show MeSH
Related in: MedlinePlus