Please use this identifier to cite or link to this item: doi:10.22028/D291-34584
Title: Targeted Lipidomics of Mitochondria in a Cellular Alzheimer’s Disease Model
Author(s): Kurokin, Irina
Lauer, Anna Andrea
Janitschke, Daniel
Winkler, Jakob
Theiss, Elena Leoni
Griebsch, Lea Victoria
Pilz, Sabrina Melanie
Matschke, Veronika
van der Laan, Martin
Grimm, Heike Sabine
Hartmann, Tobias
Grimm, Marcus Otto Walter
Language: English
Title: Biomedicines
Volume: 9
Issue: 8
Publisher/Platform: MDPI
Year of Publication: 2021
Free key words: mitochondria
Alzheimer’s disease
neurodegeneration
lipidomics
unsaturated fatty acids
phosphatidylcholine
phosphatidylethanolamine
lyso-phospholipids
plasmalogens
carnitine carrier system
DDC notations: 610 Medicine and health
Publikation type: Journal Article
Abstract: Alzheimer’s disease (AD) is neuropathologically characterized by the accumulation of Amyloid-β (Aβ) in senile plaques derived from amyloidogenic processing of a precursor protein (APP). Recently, changes in mitochondrial function have become in the focus of the disease. Whereas a link between AD and lipid-homeostasis exists, little is known about potential alterations in the lipid composition of mitochondria. Here, we investigate potential changes in the main mitochondrial phospholipid classes phosphatidylcholine, phosphatidylethanolamine and the corresponding plasmalogens and lyso-phospholipids of a cellular AD-model (SH-SY5Y APPswedish transfected cells), comparing these results with changes in cell-homogenates. Targeted shotgun-lipidomics revealed lipid alterations to be specific for mitochondria and cannot be predicted from total cell analysis. In particular, lipids containing three and four times unsaturated fatty acids (FA X:4), such as arachidonic-acid, are increased, whereas FA X:6 or X:5, such as eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), are decreased. Additionally, PE plasmalogens are increased in contrast to homogenates. Results were confirmed in another cellular AD model, having a lower affinity to amyloidogenic APP processing. Besides several similarities, differences in particular in PE species exist, demonstrating that differences in APP processing might lead to specific changes in lipid homeostasis in mitochondria. Importantly, the observed lipid alterations are accompanied by changes in the carnitine carrier system, also suggesting an altered mitochondrial functionality
DOI of the first publication: 10.3390/biomedicines9081062
Link to this record: urn:nbn:de:bsz:291--ds-345847
hdl:20.500.11880/31657
http://dx.doi.org/10.22028/D291-34584
ISSN: 2227-9059
Date of registration: 27-Aug-2021
Description of the related object: Supplementary Materials
Related object: https://www.mdpi.com/article/10.3390/biomedicines9081062/s1
Faculty: M - Medizinische Fakultät
Department: M - Medizinische Biochemie und Molekularbiologie
M - Neurologie und Psychiatrie
Professorship: M - Prof. Dr. Tobias Hartmann
M - Prof. Dr. Martin Van der Laan
Collections:SciDok - Der Wissenschaftsserver der Universität des Saarlandes

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