Journal
PROTEOMICS
Volume 15, Issue 9, Pages 1574-1586Publisher
WILEY
DOI: 10.1002/pmic.201400277
Keywords
Aging; Bioenergetics; Brain mitochondria; Quantitative proteomics
Funding
- NIH [P30 MH06221, R01 MH073490]
Ask authors/readers for more resources
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 as determinants of normal healthy aging. Here the global changes concomitant with aging in the mitochondrial proteome of mouse brain analyzed by quantitative mass-spectrometry based super-SILAC identified differentially expressed proteins involved in several metabolic pathways including glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation. Despite these changes, the bioenergetic function of these mitochondria was preserved. Overall, this data indicates that proteomic changes during aging may compensate for functional defects aiding in preservation of mitochondrial function. The mass spectrometry proteomics data have been deposited to the ProteomeXchange Consortium with the data set identifier PXD001370 ().
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available