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Exercise Training Upregulates Mitochondrial Survival Proteins BAG‐4 and Thioredoxin‐2 in the Aging Rat Heart
Author(s) -
Lawler John M,
Kwak HyoBum,
Kim JongHee
Publication year - 2008
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.22.1_supplement.753.8
Subject(s) - downregulation and upregulation , apoptosis , endurance training , oxidative stress , ventricle , thioredoxin , treadmill , medicine , sed , endocrinology , mitochondrion , chemistry , biology , microbiology and biotechnology , biochemistry , gene
Recently, we showed that in the rat heart exercise training (ET) reduces age‐induced oxidative stress, apoptosis, caspase‐3 cleavage, and upstream modulation of mitochondrial Bcl‐2 signaling by increasing anti‐apoptotic Bcl‐2 and decreasing pro‐apoptotic Bax. BAG‐4 and thioredoxin‐2 (Trx2) are mitochondrial survival proteins that promote protection against apoptosis by binding or stimulating Bcl‐2 and Bcl‐XL. The purpose of this study was to test the hypothesis that 12 weeks of endurance exercise training would upregulate levels of survival proteins BAG‐4 and Trx2 in the aging rat heart. Three and 31 mo. old Fischer 344 x Brown Norway F1 rats were assigned to young sedentary (YS), young exercise (YE), old sedentary (OS), or old exercise (OE) groups. ET groups ran on a treadmill at 20 m/min (young) or 10 m/min (old), 18% grade, 45 min/day, 5 day/wk for 12 wks, and left ventricle (LV) samples were extracted from all groups after ET. Active BAG‐4 levels decreased by 66% with aging in the LV, but were increased (+121%) by exercise in the OE group. ET‐induced upregulation of active BAG‐4 in OE rats was directly related a 139% increase in the pro‐form of BAG‐4. Trx2 protein levels were 75% and 78% higher in LV from the YE and OE groups, compared to the YS and OS groups. Our data indicate the mitochondrial survival proteins BAG‐4 and Trx2 are inducible with endurance training in the old rat heart, and offer putative therapeutic targets.