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Updated: May 27, 2025
Differentiation of the SH-SY5Y Human Neuroblastoma Cell Line
Published on: February 17, 2016
Sub-network transcriptome dataset for diseases associated with exposure to bisphenol F and bisphenol S in human
Andrea Guzman1, Christina L Sanchez1, Emma Ivantsova1
1Center for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, UF Genetics Institute, Interdisciplinary Program in Biomedical Sciences Neuroscience, University of Florida, Gainesville, FL 32611, USA.
Abstract:
Bisphenol A replacement chemicals can result in toxicity to neuronal cells, however, the underlying mechanisms are not well characterized. Transcriptome analysis was conducted in the neuronal SH-SY5Y human cell line following exposure of cells to either bisphenol F (BPF) or bisphenol S (BPS) at a concentration of 0.1 nM. Transcriptome data were used to predict which diseases were associated with bisphenol exposure using sub-network enrichment analysis. There were 305 subnetworks perturbed by BPF and 279 subnetworks perturbed by BPS. Top gene sets altered by BPF included urticaria, gastric lesion, attention deficit disorder, familial Mediterranean fever, malocclusion, and lupus erythematosus while for BPS, top gene sets included chronic urticaria, polymyositis, genital herpes, and hypergammaglobulinemia. There were 164 common diseases identified between BPF and BPS datasets. These included protein regulators of androgen deficiency, cerebral toxoplasmosis, metabolic alkalosis, panic attack, T-helper lymphocyte infiltration and vitiligo. Data can be re-used in regulatory toxicology to characterize biomarkers of exposure and elucidate common molecular responses to bisphenol replacements.
Insights
Bisphenol F (BPF) and Bisphenol S (BPS) exposure in neuronal cells may lead to various diseases. These bisphenol replacements share common molecular responses and potential disease associations, impacting regulatory toxicology.
Area of Science:
- Toxicology
- Neuroscience
- Genomics
Background:
- Bisphenol A (BPA) replacements are increasingly used, but their neurotoxicity mechanisms remain unclear.
- Neuronal cell toxicity from BPA alternatives necessitates understanding their molecular effects.
Purpose of the Study:
- To investigate the molecular mechanisms of neurotoxicity induced by bisphenol F (BPF) and bisphenol S (BPS).
- To identify potential disease associations and common molecular responses to BPF and BPS exposure in neuronal cells.
Main Methods:
- Transcriptome analysis of human neuronal SH-SY5Y cells exposed to 0.1 nM BPF or BPS.
- Sub-network enrichment analysis to predict disease associations from transcriptome data.
Main Results:
- BPF exposure perturbed 305 subnetworks, associated with conditions like urticaria and attention deficit disorder.
- BPS exposure perturbed 279 subnetworks, linked to chronic urticaria and genital herpes.
- 164 common disease associations were identified between BPF and BPS, including metabolic alkalosis and vitiligo.
Conclusions:
- BPF and BPS elicit distinct yet overlapping molecular responses in neuronal cells.
- These findings aid in characterizing biomarkers for regulatory toxicology and understanding bisphenol replacement safety.
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