Proteomics analysis of methylglyoxal-induced neurotoxic effects in SH-SY5Y cells
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Published on: August 28, 2021
Guoyi Li1, Ming Chang, Huiyi Jiang
1Proteomics Laboratory, Department of Neurology, The First Hospital, Jilin University, Changchun, China.
Abstract:
Reactive carbonyl compounds contribute to aging, Alzheimer's disease (AD) and other neurodegenerative diseases. Among these compounds, methylglyoxal (MG) can yield advanced glycation end products (AGEs), which are crucial in AD pathogenesis. However, the molecular and biochemical mechanisms of MG neurotoxicity are not completely understood. In the present study, SH-SY5Y cells were treated with MG to induce cell death. 2-D Fluorescence Difference Gel Electrophoresis and matrix-assisted laser desorption/ionization-time of flight mass spectrometry were employed to determine the changes in protein levels in these cells compared with vehicle-treated cells. Proteomics analysis revealed that 49 proteins were differentially expressed in MG-treated SH-SY5Y cells, of which 16 were upregulated and 33 were downregulated. Among them, eight proteins were identified unambiguously. The significant changes in protein levels of actin, immunoglobulin lambda light chain and protein phosphatase 2 were noteworthy given their functional roles in AD pathogenesis. Taken together, our results suggest that multiple pathways are potentially involved in MG-induced neuron death.
Insights
Methylglyoxal (MG) causes neuron death by altering protein levels, contributing to aging and Alzheimer's disease (AD). This study identified 49 differentially expressed proteins, revealing pathways involved in MG neurotoxicity.
Area of Science:
- Neuroscience
- Biochemistry
- Proteomics
Background:
- Reactive carbonyl compounds, like methylglyoxal (MG), are implicated in aging and neurodegenerative diseases such as Alzheimer's disease (AD).
- MG can form advanced glycation end products (AGEs), which play a significant role in AD pathogenesis.
- The precise molecular mechanisms underlying MG-induced neurotoxicity remain incompletely understood.
Purpose of the Study:
- To investigate the proteomic changes in SH-SY5Y cells induced by methylglyoxal (MG).
- To identify specific proteins and pathways affected by MG treatment, contributing to the understanding of MG neurotoxicity in the context of Alzheimer's disease.
Main Methods:
- SH-SY5Y cells were treated with methylglyoxal (MG) to induce cell death.
- Proteomic analysis using 2-D Fluorescence Difference Gel Electrophoresis and MALDI-TOF MS was performed.
- Differential protein expression levels were compared between MG-treated and vehicle-treated cells.
Main Results:
- Proteomics analysis identified 49 differentially expressed proteins in MG-treated SH-SY5Y cells.
- Of these, 16 proteins were upregulated and 33 were downregulated.
- Significant changes were observed in actin, immunoglobulin lambda light chain, and protein phosphatase 2, proteins relevant to AD pathogenesis.
Conclusions:
- Methylglyoxal (MG) treatment leads to significant alterations in cellular protein expression in neurons.
- These proteomic changes suggest the involvement of multiple pathways in MG-induced neuron death.
- The identified protein changes provide insights into the molecular mechanisms of MG neurotoxicity relevant to Alzheimer's disease.
