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Neuroprotective Effects of Protein Tyrosine Phosphatase 1B Inhibition against ER Stress-Induced Toxicity

Title
Neuroprotective Effects of Protein Tyrosine Phosphatase 1B Inhibition against ER Stress-Induced Toxicity
Authors
Jeon, Yu-MiLee, ShinryeKim, SeyeonKwon, YounghwiKim, KiyoungChung, Chang GeonLee, SeongsooLee, Sung BaeKim, Hyung-Jun
DGIST Authors
Chung, Chang Geon; Lee, Sung Bae
Issue Date
2017-04
Citation
Molecules and Cells, 40(4), 280-290
Type
Article
Article Type
Article
Keywords
Cortical NeuronsDeathEndoplasmic Reticulum Stress (ER Stress)Endoplasmic Reticulum Stress (ER Stress)Endoplasmic Reticulum Stress (ER Stress)Metabolic DiseaseMg132Neuroblastoma CellsNeurotrophic FactorOxidative StressProteasomePTP1BReactive Oxygen Species (ROS)Reactive Oxygen Species (ROS)RotenoneRotenoneUbiquitin Proteasome SystemUbiquitin Proteasome SystemUp Regulation
ISSN
1016-8478
Abstract
Several lines of evidence suggest that endoplasmic reticulum (ER) stress plays a critical role in the pathogenesis of many neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Protein tyrosine phosphatase 1B (PTP1B) is known to regulate the ER stress signaling pathway, but its role in neuronal systems in terms of ER stress remains largely unknown. Here, we showed that rotenone-induced toxicity in human neuroblastoma cell lines and mouse primary cortical neurons was ameliorated by PTP1B inhibition. Moreover, the increase in the level of ER stress markers (eIF2α phosphorylation and PERK phosphorylation) induced by rotenone treatment was obviously suppressed by concomitant PTP1B inhibition. However, the rotenone-induced production of reactive oxygen species (ROS) was not affected by PTP1B inhibition, suggesting that the neuroprotective effect of the PTP1B inhibitor is not associated with ROS production. Moreover, we found that MG132-induced toxicity involving proteasome inhibition was also ameliorated by PTP1B inhibition in a human neuroblastoma cell line and mouse primary cortical neurons. Consistently, downregulation of the PTP1B homologue gene in Drosophila mitigated rotenone-and MG132-induced toxicity. Taken together, these findings indicate that PTP1B inhibition may represent a novel therapeutic approach for ER stress-mediated neurodegenerative diseases. © The Korean Society for Molecular and Cellular Biology. All rights reserved.
URI
http://hdl.handle.net/20.500.11750/4208
DOI
10.14348/molcells.2017.2320
Publisher
Korean Society for Molecular and Cellular Biology
Related Researcher
  • Author Lee, Sung Bae SB LAB(Lab of Neurodegenerative diseases and Aging)
  • Research Interests Cellular mechanism of neurodegenerative diseases; Neuronal maintenance and remodeling; 퇴행성 뇌질환의 세포기전; 신경계 유지 및 리모델링 연구
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Collection:
Brain and Cognitive SciencesETC1. Journal Articles


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