Proteomics

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Quantitative Proteomic Analysis of an Alexander Disease Murine Model with Severe Reactive Gliosis

ABSTRACT: We performed label-free micro-data-independent acquisition (µDIA) to assay brain proteins from a severe model of Alexander disease (AxD, lethal at postnatal day ~35). Of the 5,005 proteins quantified, we observed upregulation of adipocytokine signaling, PPAR, insulin resistance, and glutathione pathways with concomitant downregulation of platelet activation, ether lipid synthesis, and steroid biosynthesis pathways. To validate these DIA results, we setup a targeted parallel reaction monitoring-mass spectrometry assay (PRM-MS) for selected proteins with altered relative concentrations. The PRM-MS assays confirmed the upward or downward relative concentration differences in 16/16 (100%) of the proteins targeted, with 15/16 (94%) of these proteins reaching statistical significance (P-value < 0.05).

INSTRUMENT(S): Orbitrap Fusion Lumos, Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain

SUBMITTER: Michael Heaven  

LAB HEAD: Michelle L Olsen

PROVIDER: PXD021884 | Pride | 2021-11-30

REPOSITORIES: Pride

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Dataset's files

Source:
Action DRS
DescriptionofuDIAandPRMrawfilesbiologicalconditionAxDorwildtype.xlsx Xlsx
FL20171222_Olsen-AXD-DIA1.raw Raw
FL20171222_Olsen-AXD-DIA2.raw Raw
FL20171222_Olsen-AXD-DIA3.raw Raw
FL20171222_Olsen-AXD-DIA4.raw Raw
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Publications

Metabolic Enzyme Alterations and Astrocyte Dysfunction in a Murine Model of Alexander Disease With Severe Reactive Gliosis.

Heaven Michael R MR   Herren Anthony W AW   Flint Daniel L DL   Pacheco Natasha L NL   Li Jiangtao J   Tang Alice A   Khan Fatima F   Goldman James E JE   Phinney Brett S BS   Olsen Michelle L ML  

Molecular & cellular proteomics : MCP 20211120 1

Alexander disease (AxD) is a rare and fatal neurodegenerative disorder caused by mutations in the gene encoding glial fibrillary acidic protein (GFAP). In this report, a mouse model of AxD (GFAP<sup>Tg</sup>;Gfap<sup>+/R236H</sup>) was analyzed that contains a heterozygous R236H point mutation in murine Gfap as well as a transgene with a GFAP promoter to overexpress human GFAP. Using label-free quantitative proteomic comparisons of brain tissue from GFAP<sup>Tg</sup>;Gfap<sup>+/R236H</sup> versu  ...[more]

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