Proteomics

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Proteomic analysis of mitochondria isolated from the frontal cortex and hippocampus of apolipoprotein E knockout mice treated with Alda-1, an activator of mitochondrial aldehyde dehydrogenase (ALDH2)

ABSTRACT: Recently, it has been shown that mitochondrial dysfunction and oxidative stress play important roles in the pathogenesis of neurodegeneration. Mitochondrial aldehyde dehydrogenase (ALDH2), an enzyme responsible for the detoxification of reactive aldehydes – the end products of lipid peroxidation, is considered to exert protective function in mitochondria. The aim of our study was to use the methods of differential proteomics in concert with molecular and morphological techniques to elucidate the changes in the frontal cortex and hippocampus of apolipoprotein E knockout (apoE-/-) mice (an animal model of the early stages of Alzheimer’s disease) upon treatment with Alda-1 – a small molecular weight activator of ALDH2.

INSTRUMENT(S): LTQ

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain

SUBMITTER: Aneta Stachowicz  

LAB HEAD: Rafał Olszanecki

PROVIDER: PXD004022 | Pride | 2017-02-23

REPOSITORIES: Pride

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Publications

Proteomic Analysis of Mitochondria-Enriched Fraction Isolated from the Frontal Cortex and Hippocampus of Apolipoprotein E Knockout Mice Treated with Alda-1, an Activator of Mitochondrial Aldehyde Dehydrogenase (ALDH2).

Stachowicz Aneta A   Olszanecki Rafał R   Suski Maciej M   Głombik Katarzyna K   Basta-Kaim Agnieszka A   Adamek Dariusz D   Korbut Ryszard R  

International journal of molecular sciences 20170217 2

The role of different genotypes of apolipoprotein E (apoE) in the etiology of Alzheimer's disease is widely recognized. It has been shown that altered functioning of apoE may promote 4-hydroxynonenal modification of mitochondrial proteins, which may result in mitochondrial dysfunction, aggravation of oxidative stress, and neurodegeneration. Mitochondrial aldehyde dehydrogenase (ALDH2) is an enzyme considered to perform protective function in mitochondria by the detoxification of the end products  ...[more]

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