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Age-related proteostasis and metabolic alterations in Caspase-2-deficient mice.

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journal contribution
posted on 2015-01-01, 00:00 authored by C H Wilson, S Shalini, A Filipovska, T R Richman, S Davies, Sheree MartinSheree Martin, Sean McgeeSean Mcgee, J Puccini, A Nikolic, L Dorstyn, S Kumar
Ageing is a complex biological process for which underlying biochemical changes are still largely unknown. We performed comparative profiling of the cellular proteome and metabolome to understand the molecular basis of ageing in Caspase-2-deficient (Casp2(-/-)) mice that are a model of premature ageing in the absence of overt disease. Age-related changes were determined in the liver and serum of young (6-9 week) and aged (18-24 month) wild-type and Casp2(-/-) mice. We identified perturbed metabolic pathways, decreased levels of ribosomal and respiratory complex proteins and altered mitochondrial function that contribute to premature ageing in the Casp2(-/-) mice. We show that the metabolic profile changes in the young Casp2(-/-) mice resemble those found in aged wild-type mice. Intriguingly, aged Casp2(-/-) mice were found to have reduced blood glucose and improved glucose tolerance. These results demonstrate an important role for caspase-2 in regulating proteome and metabolome remodelling during ageing.

History

Journal

Cell Death and Disease

Volume

6

Pagination

e1597 - e1597

Publisher

Nature Publishing Group

Location

England

eISSN

2041-4889

Language

eng

Publication classification

C Journal article; C1 Refereed article in a scholarly journal

Copyright notice

2015, Nature Publishing Group

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