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Aging alters the mitochondrial stress response
Author(s) -
Haak Jodie,
Kregel Kevin
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.617.16
Subject(s) - hsp60 , mitochondrion , heat shock protein , hsp70 , microbiology and biotechnology , biology , heat shock , chemistry , biochemistry , gene
The mitochondrial stress response involves a set of stress proteins known as heat shock proteins (Hsps) that repair and restrict protein damage in the mitochondria. Specifically, Hsp60, Hsp10, and mitochondrial Hsp70 (mtHsp70) are members of the mitochondrial stress protein arsenal. While it has been established that aging impairs the cell stress response, the effect of age on mitochondrial stress proteins remains unknown. To examine the effect of age on the mitochondrial stress response, young (6 mo) and old (24 mo) Fischer 344 rats were heat stressed (41.0°C for 30 min) on two consecutive days, and their liver mitochondria were isolated at 2 and 24 h after the second stress. Immunoblotting revealed that mitochondria exhibit altered stress protein expression after heat stress. The differences in protein levels were most notable in Hsp60, the main heat‐inducible mitochondrial stress protein. Hsp60 protein levels increased significantly 2 h after heating in young mitochondria and remained elevated 24 h after heating. In old mitochondria, a delayed and blunted elevation in Hsp60 levels was observed as compared to young. Additionally, mtHsp70 and Hsp10 protein levels increased solely in young and not old liver mitochondria in response to stress. These data indicate that aging causes mitochondria to lose their ability to respond properly to physiological stress. (Supported by NIH AG12350)