O-GlcNAc protein modification in C2C12 myoblasts exposed to oxidative stress indicates parallels with endogenous antioxidant defense

Peternelj, Tina Tinkara, Marsh, Susan A., Morais, Christudas, Small, David M., Dalbo, Vincent J., Tucker, Patrick S. and Coombes, Jeff S. (2014) O-GlcNAc protein modification in C2C12 myoblasts exposed to oxidative stress indicates parallels with endogenous antioxidant defense. Biochemistry and Cell Biology, 93 1: 63-73. doi:10.1139/bcb-2014-0106

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Author Peternelj, Tina Tinkara
Marsh, Susan A.
Morais, Christudas
Small, David M.
Dalbo, Vincent J.
Tucker, Patrick S.
Coombes, Jeff S.
Title O-GlcNAc protein modification in C2C12 myoblasts exposed to oxidative stress indicates parallels with endogenous antioxidant defense
Journal name Biochemistry and Cell Biology   Check publisher's open access policy
ISSN 1208-6002
0829-8211
Publication date 2014
Sub-type Article (original research)
DOI 10.1139/bcb-2014-0106
Open Access Status
Volume 93
Issue 1
Start page 63
End page 73
Total pages 11
Place of publication Ottawa, ON, Canada
Publisher National Research Council of Canada
Collection year 2015
Language eng
Abstract A growing body of evidence demonstrates the involvement of protein modification with O-linked -N-acetylglucosamine (O-GlcNAc) in the stress response and its beneficial effects on cell survival. Here we investigated protein O-GlcNAcylation in skeletal muscle cells exposed to oxidative stress and the crosstalk with endogenous antioxidant system. The study focused on antioxidant enzymes superoxide dismutase 2 (SOD2), catalase (CAT), and glutathione peroxidase 1 (GPX1), and transcriptional regulators proliferator-activated receptor gamma coactivator 1- (PGC-1) and forkhead box protein O1 (FOXO1), which play important roles in oxidative stress response and are known to be O-GlcNAc-modified. C2C12 myoblasts were subjected to 24 h incubation with different reagents, including hydrogen peroxide, diethyl maleate, high glucose, and glucosamine, and the inhibitors of O-GlcNAc cycling enzymes. Surprisingly, O-GlcNAc levels were significantly increased only with glucosamine, whilst other treatments showed no effect. Significant changes at the mRNA level were observed with concomitant upregulation of the genes for O-GlcNAc enzymes and stress-related proteins with oxidizing agents and downregulation of these genes with agents promoting O-GlcNAcylation. Our findings suggest a role of O-GlcNAc in the stress response and indicate an inhibitory mechanism controlling O-GlcNAc levels in the muscle cells. This could represent an important homeostatic regulation of the cellular defense system. K
Keyword Adaptive response
Antioxidant enzyme
Myoblasts
O-GlcNAc
Oxidant
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
School of Human Movement and Nutrition Sciences Publications
School of Medicine Publications
 
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