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Environmental Pollutant PCB 153 Is Associated with Candidate Alternative Splicing Alterations in Intellectual Disability-Associated Genes: An Exploratory RNA-Seq Splicing Analysis in a Neuronal Model.

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PCB 153 Modulates Genes Involved in Proteasome and Neurodegeneration-Related Pathways in Differentiated SH-SY5Y

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Polychlorinated biphenyls (PCBs) disrupt protein homeostasis in neuronal cells, triggering proteasome responses. This early molecular alteration may contribute to neurodegenerative disease mechanisms.

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PCB 153environmental pollutantsexposure assessmentneurotoxicity mechanismspolychlorinated biphenylsrisk characterizationtranscriptomic analysis

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Area of Science:

  • Environmental toxicology
  • Neuroscience
  • Molecular biology

Background:

  • Polychlorinated biphenyls (PCBs) are persistent environmental contaminants linked to neurotoxicity and neurodegenerative diseases.
  • PCB 153, a prevalent congener, bioaccumulates and disrupts cellular homeostasis.
  • Understanding early molecular effects of PCB 153 is crucial for neuroprotection.

Purpose of the Study:

  • To investigate the transcriptomic alterations induced by sub-cytotoxic concentrations of PCB 153 in differentiated neuronal cells.
  • To identify early molecular events associated with PCB 153 exposure that may precede neurodegeneration.
  • To explore the impact of PCB 153 on protein homeostasis pathways.

Main Methods:

  • SH-SY5Y neuronal cells were differentiated and exposed to varying concentrations of PCB 153.
  • Cell viability was assessed using MTT assay.
  • RNA-sequencing (RNA-Seq) was performed on cells treated with the highest non-cytotoxic PCB 153 dose (5 μM).
  • Differential gene expression analysis was conducted using DESeq2.
  • Functional enrichment analysis utilized Gene Ontologies and KEGG pathways.
  • Western blot validated protein level changes.

Main Results:

  • RNA-Seq identified 1882 significantly altered genes (q-value < 0.05) in response to PCB 153.
  • Gene Ontology analysis revealed significant enrichment of proteasome-related terms, with coordinated upregulation of proteasomal subunits.
  • KEGG pathway analysis highlighted significant enrichment of pathways associated with Alzheimer's, Parkinson's, and ALS.
  • Western blot confirmed changes in protein levels for selected targets.

Conclusions:

  • PCB 153 exposure induces a robust proteostatic response in neuronal cells, characterized by proteasome activation.
  • These findings suggest that PCB 153 disrupts protein homeostasis at a molecular level, potentially contributing to neurodegenerative processes.
  • Early transcriptomic changes provide insights into the mechanisms underlying PCB-induced neurotoxicity.