PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
February 8, 2026Scientific Data0 citationsOpen Access

Chromatin accessibility and transcriptome in human neuronal model exposed to Parkinson’s environmental toxins

JHJingchao HongJHJuanjuan Huang

Key Points

  • To investigate how environmental toxins affect chromatin accessibility and gene expression in a neuronal model relevant to Parkinson's disease.
  • Utilized human neuroblastoma cell line SH-SY5Y as a neuronal model
  • Exposed cells to Parkinson's-related environmental toxins rotenone and MPP⁺
  • Conducted RNA sequencing (RNA-seq) for transcriptome profiling
  • Performed Assay for Transposase-Accessible Chromatin sequencing (ATAC-seq) to assess chromatin accessibility
  • Characterized specific alterations in chromatin accessibility due to toxin exposure
  • Mapped genome-wide chromatin accessibility landscapes
  • Generated comprehensive data resource linking gene expression with chromatin dynamics
  • Identified potential targets for biomarker discovery related to environmentally linked sporadic Parkinson’s disease.

Abstract

Parkinson's disease (PD) is a complex neurodegenerative disorder where environmental factors play a predominant role in sporadic cases. While environmental toxins are implicated in PD pathogenesis via epigenetic pathways, the specific alterations in chromatin accessibility induced by these toxins remain poorly characterized. To address this gap, we established in vitro models using the human neuroblastoma cell line SH-SY5Y, a well-established neuronal model, exposed to the PD-associated environmental toxins rotenone and MPP⁺. We performed RNA sequencing (RNA-seq) to profile the transcriptome and Assay for Transposase-Accessible Chromatin sequencing (ATAC-seq) to map genome-wide chromatin accessibility landscapes under toxin-exposed conditions. This integrated dataset provides a comprehensive resource detailing both gene expression and chromatin accessibility dynamics in response to PD-relevant environmental neurotoxins and will facilitate investigations into transcriptional regulation, biomarker discovery, and the epigenetic basis of environmentally linked sporadic PD.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Hong et al. (2026) studied this question.

synapsesocial.com/papers/698827c90fc35cd7a8846c6chttps://doi.org/10.1038/s41597-026-06626-4
Ask AI
Helpful
Bookmark
Share
View Full Paper