Dataset Information

Aging Mouse Brain Mitochondria LC-MS/MS

ABSTRACT: This study investigates the proteomic alterations in brain mitochondria isolated from 5- (mature), 12- (old), and 24-month-old (aged) mice to examine normal "healthy" aging. Using quantitative mass-spectrometry based super-SILAC, our findings revealed global proteomic changes in brain mitochondria identifying several metabolic pathways including glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation. Overall, we found that the bioenergetic function of these mitochondria was preserved suggesting the proteomic alterations potentially allow for compensatory mechanisms to combat aging.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain

SUBMITTER: Kelly Stauch

LAB HEAD: Howard Fox

PROVIDER: PXD001370 | Pride | 2015-01-27

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	02Sept14_SILAC_24month_mouse_WBMito_1_2_3_grouped.group	Other
	02Sept14_SILAC_24month_mouse_WBMito_1_2_3_grouped_PeptideSummary.txt	Txt
	02Sept14_SILAC_24month_mouse_WBMito_1_2_3_grouped_ProteinSummary.txt	Txt
	02Sept14_SILAC_24month_mouse_WBMito_1_2_3_grouped__FDR.xlsx	Xlsx
	04Jun13_24month_mouse_WBMito_2A.wiff	Wiff

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Publications

Proteomic analysis and functional characterization of mouse brain mitochondria during aging reveal alterations in energy metabolism.

Stauch Kelly L KL Purnell Phillip R PR Villeneuve Lance M LM Fox Howard S HS

Proteomics 20150210 9

Mitochondria are the main cellular source of reactive oxygen species and are recognized as key players in several age-associated disorders and neurodegeneration. Their dysfunction has also been linked to cellular aging. Additionally, mechanisms leading to the preservation of mitochondrial function promote longevity. In this study we investigated the proteomic and functional alterations in brain mitochondria isolated from mature (5 months old), old (12 months old), and aged (24 months old) mice a ...[more]

PMID: 25546256

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Project description:Functional decline and structural alterations of the brain microvasculature are associated with cognitive impairment and development of dementias such as Alzheimer’s disease during aging. Although mechanisms of leading to microvascular changes during aging are not clear, the loss of mitochondria and reduced efficiency of remaining mitochondria appear to play a major role. While pharmacological agents which target mitochondria such as SS-31 have been shown to be effective in beneficial during aging and diseases, the full extent on mitochondrial- and non-mitochondrial proteins in the brain microvasculature has not been examined. We tested the hypothesis that attenuation of aging-associated changes in the brain microvascular proteome via targeting mitochondria represents a therapeutic option in the aging brain. We used male, aged (>18 months) C57Bl6/J mice treated with a mitochondria-targeted tetrapeptide, SS-31 or vehicle saline. Baseline cerebral blood flow (CBF) was determined using laser speckle imaging during the two-week treatment period. Then, isolated cortical microvessels (MVs), composed of end arterioles, capillaries, and venules, were used for Orbitrap Eclipse Tribrid mass spectrometry. Baseline CBF was similar between the groups, whereas bioinformatic analysis revealed substantial differences in protein abundance of cortical MVs between SS-31 and vehicle groups. Specifically, we identified 6,266 proteins in our data set from which 12% were mitochondrial or mitochondria associated. 107 of these proteins were significantly differentially expressed between the treatment and vehicle groups, and were associated with the oxidative phosphorylation, metabolism, antioxidant defense system, or mitochondrial dynamics. Administration of SS-31 also affected many non-mitochondrial proteins. Our findings suggest that mitochondria in the microvasculature represent a therapeutic target in the aging brain, and widespread changes in the proteome may underlie the mechanisms of rejuvenating actions of SS-31 in the aging phenotype.