Autor: |
Magalingam KB; Jeffrey Cheah School of Medicine and Health Sciences, Monash University, Bandar Sunway 47500, Malaysia., Somanath SD; Pathology Division, School of Medicine, International Medical University, Kuala Lumpur 57000, Malaysia., Radhakrishnan AK; Jeffrey Cheah School of Medicine and Health Sciences, Monash University, Bandar Sunway 47500, Malaysia. |
Jazyk: |
angličtina |
Zdroj: |
Experimental neurobiology [Exp Neurobiol] 2023 Jun 30; Vol. 32 (3), pp. 119-132. |
DOI: |
10.5607/en22035 |
Abstrakt: |
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. |
Databáze: |
MEDLINE |
Externí odkaz: |
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