RT Journal Article
SR Electronic
A1 Ding, Nan
A1 Peng, Peng
A1 Chu, Yu-Jing
A1 Wang, Jing-Jing
A1 Chen, Shu-Yi
A1 Arulthas, Renuka
A1 Deng, Yan-Qiu
T1 The effects of O-GlcNAc alteration on Alzheimer-like neurodegeneration in SK-N-SH cells
JF Biomedical papers
YR 2018
VO 162
IS 3
SP 243
OP 248
DO 10.5507/bp.2018.042
UL https://biomed.papers.upol.cz/artkey/bio-201803-0013.php
AB Background:  O-GlcNAcylation is a highly dynamic post-translational modification that plays a key role in regulating phosphorylation of protein and cell survival. The proteins O-GlcNAcylation level is regulated dynamically by O-GlcNAc transferase (OGT) and β-N-acetylglucosaminidase (O-GlcNAcase, OGA). Although previous studies have suggested the role of O-GlcNAcylation in neurodegenerative diseases, the mechanism of O-GlcNAcylation in Alzheimer's disease (AD) remains unclear. Methods: The decrease of O-GlcNAcylation by alloxan, an OGT inhibitor, and increase by NAG-thiazolines (NAG-Ae), an O-GlcNAcase inhibitor were tested to investigate the effects of O-GlcNAc alteration on AD like neurodegeneration in SK-N-SH cells. Results: The level of O-GlcNAcylation was decreased in alloxan treated cells and increased in NAG-Ae treated cells. Meanwhile, it was observed that both abnormal phosphorylation of NFs in cell bodies and apoptosis induced by alloxan treatment can be resisted by pretreatment or simultaneous treatment with appropriate NAG-Ae. Conclusion:  These results demonstrated that increasing O-GlcNAc with NAG-Ae protected AD like neurodegeneration from NFs hyperphosphorylation and the cell loss, suggesting the role of O-GlcNAc in the pathogenesis and therapy of AD.