Detection of cardiac O-GlcNAcylation via subcellular fractionation and dual antibody analysis in pressure overload cardiac hypertrophy

通过亚细胞分级分离和双抗体分析检测压力负荷过重性心肌肥厚中的心脏 O-GlcNAc 修饰

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Abstract

Protein O-GlcNAcylation is a dynamic post-translational modification with emerging roles in cardiac pathophysiology. The availability of different pan-specific antibodies to assess global O-GlcNAc levels, and variability in western blot results has hindered cross-study reproducibility and interpretation. In this study, we applied optimized immunoblotting protocols using both CTD110.6 and RL2 O-GlcNAc antibodies, alongside subcellular fractionation, to investigate temporal and sex-specific changes in cardiac O-GlcNAcylation during pressure overload hypertrophy (POH) from transverse aortic constriction (TAC) during early (1-week POH, 1wTAC) and chronic (6-weeks POH, 6wTAC) POH in mice. Global O-GlcNAc levels were elevated in early POH and returned to baseline in chronic POH, consistent across both antibodies and sexes. Subcellular fractionation revealed persistent O-GlcNAc elevations in cytoplasmic and membrane fractions in chronic POH for both sexes, which were not detected in unfractionated samples. Female mice exhibited significantly higher O-GlcNAc levels than males during POH, particularly at early POH, highlighting sex-specific regulation. OGT and OGA protein levels also varied by compartment and sex, suggesting differential enzymatic control. In conclusion, our findings underscore the importance of methodological rigor in O-GlcNAc detection and demonstrate that fractionation enhances sensitivity to subtle changes in cardiac O-GlcNAcylation. Our principal new findings are protein O-GlcNAcylation dysregulation continues from early POH (1wTAC) into chronic POH (6wTAC groups) along with showing differences in O-GlcNAc levels between males and females during POH. These results provide new insights into the temporal and sex-dependent dynamics of O-GlcNAc signaling in POH and support its potential as a therapeutic target in cardiovascular disease.

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