Manganese-Induced Neurotoxicity and Alterations in Gene Expression in Human Neuroblastoma SH-SY5Y Cells

Manganese (Mn) is an essential trace element required for many physiological functions including proper biochemical and cellular functioning of the central nervous system (CNS). However, exposure to excess level of Mn through occupational settings or from environmental sources has been associated wi...

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Bibliographic Details
Published in:Biological trace element research 2018-06, Vol.183 (2), p.245-253
Main Authors: Gandhi, Deepa, Sivanesan, Saravanadevi, Kannan, Krishnamurthi
Format: Article
Language:English
Subjects:
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Apoptosis
Biochemistry
Biomedical and Life Sciences
Biotechnology
Cell death
Cells
Central nervous system
Cluster analysis
DNA microarrays
Exposure
Gene expression
Genes
Lethal limits
Life Sciences
Manganese
Molecular chains
Molecular modelling
Neuroblastoma
Neuroblasts
Neurogenesis
Neurotoxicity
Nutrition
Occupational exposure
Oncology
p53 Protein
Physiological functions
Receptors
Signal transduction
Signaling
Synaptic transmission
Synaptogenesis
Toxicity
Trace elements
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Summary:Manganese (Mn) is an essential trace element required for many physiological functions including proper biochemical and cellular functioning of the central nervous system (CNS). However, exposure to excess level of Mn through occupational settings or from environmental sources has been associated with neurotoxicity. The cellular and molecular mechanism of Mn-induced neurotoxicity remains unclear. In the current study, we investigated the effects of 30-day exposure to a sub-lethal concentration of Mn (100 μM) in human neuroblastoma cells (SH-SY5Y) using transcriptomic approach. Microarray analysis revealed differential expression of 1057 transcripts in Mn-exposed SH-SY5Y cells as compared to control cells. Gene functional annotation cluster analysis exhibited that the differentially expressed genes were associated with several biological pathways. Specifically, genes involved in neuronal pathways including neuron differentiation and development, regulation of neurogenesis, synaptic transmission, and neuronal cell death (apoptosis) were found to be significantly altered. KEGG pathway analysis showed upregulation of p53 signaling pathways and neuroactive ligand-receptor interaction pathways, and downregulation of neurotrophin signaling pathway. On the basis of the gene expression profile, possible molecular mechanisms underlying Mn-induced neuronal toxicity were predicted.
ISSN:0163-4984
1559-0720
DOI:10.1007/s12011-017-1153-5