The effects of O-GlcNAc alteration on Alzheimer-like neurodegeneration in SK-N-SH cells
| Autor: | Peng Peng, Yanqiu Deng, Shu-Yi Chen, Nan Ding, Yu-jing Chu, Jing-Jing Wang, Renuka Arulthas |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Hyperphosphorylation lcsh:Medicine Apoptosis N-Acetylglucosaminyltransferases General Biochemistry Genetics and Molecular Biology Pathogenesis 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Alzheimer Disease o-glcnac transferase Cell Line Tumor Alloxan neurofilament phosphorylation medicine Humans Transferase Enzyme Inhibitors Phosphorylation Cell Death business.industry Neurodegeneration lcsh:R Acetylation o-glcnacase medicine.disease o-glcnacylation beta-N-Acetylhexosaminidases Cell loss Cell biology 030104 developmental biology chemistry alzheimer's disease business 030217 neurology & neurosurgery |
| Zdroj: | Biomedical Papers, Vol 162, Iss 3, Pp 243-248 (2018) |
| ISSN: | 1804-7521 1213-8118 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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