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- W1569196623 abstract "Increased nuclear protein O-linked β-N-acetylglucosamine glycosylation (O-GlcNAcylation) mediated by high glucose treatment or the hyperglycemia of diabetes mellitus contributes to cardiac myocyte dysfunction. Mitochondrial proteins in cardiac myocytes are also submitted to O-GlcNAcylation, however, whether excessive O-GlcNAcylation alters mitochondrial function is incompletely studied. We have previously demonstrated decreased mitochondrial calcium concentration in cardiac myocytes exposed to high glucose. We hypothesize that excessive O-GlcNAcylation may be responsible of this maladaptive phenomenon and that reducing excessive O-GlcNAcylation may return mitochondrial calcium levels to normal. Our objective was to test this hypothesis, therefore, we incubated cultured neonatal mouse myocytes in high glucose (HG, 25mM) for 72 hours and inhibited O-GlcNAcylation by adenoviral expression of a dominant negative mutant of the O-GlcNAc transferase (dnOGT). As expected, mitochondrial calcium levels were reduced by 20% after HG exposure but were returned to control values after dnOGT expression. In addition, mitochondrial calcium uptake decreased by 52% in HG and was improved by expression of dnOGT, however, did not reach control values. We examined the mitochondrial calcium uniporter (MCU) and found that it is susceptible to be O-GlcNAcylated and HG further increased O-GlcNAcylation. In conclusion, our results suggest that excessive O-GlcNAcylation in hyperglycemia alters mitochondrial calcium homeostasis by increasing O-GlcNAcylated MCU. Grant Funding Source: Supported by UC MEXUS and VA-5 I01BX001121-02-" @default.
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- W1569196623 date "2014-04-01" @default.
- W1569196623 modified "2023-09-23" @default.
- W1569196623 title "Mitochondrial calcium is decreased by high glucose and is improved by reduction of protein O‐GlcNAcylation in cardiac myocytes (1078.2)" @default.
- W1569196623 doi "https://doi.org/10.1096/fasebj.28.1_supplement.1078.2" @default.
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