Chromatin accessibility and transcriptome in human neuronal model exposed to Parkinson's environmental toxins [ATAC-Seq]
Parkinson's disease 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 to profile the transcriptome and Assay for Transposase-Accessible Chromatin sequencing 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. Overall design: SH-SY5Y cells (ATCC) were cultured in DMEM/F12 (1:1) medium (Gibco, MA, USA) supplemented with 10% fetal bovine serum (Gibco, MA, USA). Cells were plated in 6-well plates at a density of 5 × 105 cells/mL and incubated overnight at 37°C with 5% CO2. Experimental groups were treated with 5 mM MPP? (Selleck, Houston, USA) and 10 µM rotenone (Sigma, Saint Louis, USA).  Negative control (NC) wells received equivalent volumes of dimethyl sulfoxide (DMSO) vehicle (Sigma, Saint Louis, USA). After 24-hour exposure, cells were harvested for RNA sequencing and ATAC-seq analyses. Three biological replicates per group (NC, MPP?, Rotenone) were processed for RNA-seq, while two replicates per group were analyzed by ATAC-seq