title: Swim-exercised mice show a decreased level of protein O-GlcNAcylation and expression of O-GlcNAc transferase in heart.
abstract: Swim-training exercise in mice leads to cardiac remodeling associated with an improvement in contractile function. Protein O-linked N-acetylglucosamine (O-GlcNAcylation) is a posttranslational modification of serine and threonine residues capable of altering protein-protein interactions affecting gene transcription, cell signaling pathways, and general cell physiology. Increased levels of protein O-GlcNAcylation in the heart have been associated with pathological conditions such as diabetes, ischemia, and hypertrophic heart failure. In contrast, the impact of physiological exercise on protein O-GlcNAcylation in the heart is currently unknown. Swim-training exercise in mice was associated with the development of a physiological hypertrophy characterized by an improvement in contractile function relative to sedentary mice. General protein O-GlcNAcylation was significantly decreased in swim-exercised mice. This effect was mirrored in the level of O-GlcNAcylation of individual proteins such as SP1. The decrease in protein O-GlcNAcylation was associated with a decrease in the expression of O-GlcNAc transferase (OGT) and glutamine-fructose amidotransferase (GFAT) 2 mRNA. O-GlcNAcase (OGA) activity was actually lower in swim-trained than sedentary hearts, suggesting that it did not contribute to the decreased protein O-GlcNAcylation. Thus it appears that exercise-induced physiological hypertrophy is associated with a decrease in protein O-GlcNAcylation, which could potentially contribute to changes in gene expression and other physiological changes associated with exercise.
authors.affiliation: Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada. dbelke@ucalgary.ca
authors.forename: Darrell D
authors.initials: DD
authors.lastname: Belke
mesh_terms: D000117:Acetylglucosamine / Q000378:metabolism*; D000222:Adaptation, Physiological; D000818:Animals; D006332:Cardiomegaly / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D015536:Down-Regulation; D015971:Gene Expression Regulation, Enzymologic; D005945:Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing); D006031:Glycosylation; D008297:Male; D051379:Mice; D009119:Muscle Contraction; D009124:Muscle Proteins / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D017351:N-Acetylglucosaminyltransferases / Q000235:genetics / Q000378:metabolism*; D019884:Nitrogenous Group Transferases / Q000235:genetics / Q000378:metabolism; D005082:Physical Exertion; D011499:Protein Processing, Post-Translational; D012333:RNA, Messenger / Q000378:metabolism; D012694:Serine; D013550:Swimming; D013912:Threonine
chemical_list: D009124:Muscle Proteins; D012333:RNA, Messenger; D013912:Threonine; D012694:Serine; D017351:N-Acetylglucosaminyltransferases; C449880:O-GlcNAc transferase; C488522:GFPT2 protein, mouse; D019884:Nitrogenous Group Transferases; D005945:Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing); D000117:Acetylglucosamine