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자료유형
학술저널
저자정보
Magalingam Kasthuri Bai (Jeffrey Cheah School of Medicine and Health Sciences Monash University Bandar Sunway 47500 Malaysia) Somanath Sushela Devi (Pathology Division School of Medicine International Medical University Kuala Lumpur 57000 Malaysia) Radhakrishnan Ammu Kutty (Jeffrey Cheah School of Medicine and Health Sciences Monash University Bandar Sunway 47500 Malaysia)
저널정보
한국뇌신경과학회 Experimental Neurobiology Experimental Neurobiology Vol.32 No.3
발행연도
2023.6
수록면
119 - 132 (14page)
DOI
10.5607/en22035

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A cell-based model of Parkinson’s disease (PD) is a well-established in vitro experimental prototype to investigate the disease mechanism and therapeutic approach for a potential anti-PD drug. The SH-SY5Y human neuroblastoma cells and 6-OHDA combo is one of the many neurotoxininduced neuronal cell models employed in numerous neuroscience-related research for discovering neuroprotective drug compounds. Emerging studies have reported a significant correlation between PD and epigenetic alterations, particularly DNA methylation. However, the DNA methylation changes of PD-related CpG sites on the 6-OHDA-induced toxicity on human neuronal cells have not yet been reported. We performed a genome-wide association study (GWAS) using Infinium Epic beadchip array surveying 850000 CpG sites in differentiated human neuroblastoma cells exposed to 6-OHDA. We identified 236 differentially methylated probes (DMPs) or 163 differentially methylated regions (DMRs) in 6-OHDA treated differentiated neuroblastoma cells than the untreated reference group with p<0.01, Δbeta cut-off of 0.1. Among 236 DMPs, hypermethylated DMPs are 110 (47%), whereas 126 (53%) are hypomethylated. Our bioinformatic analysis revealed 3 DMRs that are significantly hypermethylated and associated with neurological disorders, namely AKT1, ITPR1 and GNG7. This preliminary study demonstrates the methylation status of PD-related CpGs in the 6-OHDA-induced toxicity in the differentiated neuroblastoma cells model.

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