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Updated: Jun 12, 2026
Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
Proteomics analysis of MPP+-induced apoptosis in SH-SY5Y cells
Hongrong Xie1, Ming Chang, Xinyu Hu
1Department of Neurology, The First Hospital, Jilin University, 71 Xinmin Street, Changchun, 130021, People's Republic of China.
Abstract:
Accumulating evidence suggests that oxidative stress plays a pivotal role in dopaminergic neurodegeneration. However, the kinds of proteins involved in the response to oxidative stress remain unclear. In the present study, SH-SY5Y cells were treated with neurotoxin 1-methyl-4-phenyl-pyridinium ion (MPP+) to induce apoptotic neuronal injury. 2D-DIGE followed by MALDI-TOF-MS was used to determine the changing protein levels. Proteomics analysis revealed that 22 proteins were differentially altered in MPP(+)-treated SH-SY5Y cells, of which 7 were up-regulated proteins and 15 were down-regulated proteins, respectively. Three protein spots were unambiguously identified as sorcin, annexin V, and ribosomal protein P0. The three proteins showed a significant increase in level, suggesting a role in MPP(+)-induced apoptosis. The functional roles of these three proteins collectively indicate that multiple mechanisms are pertinent in the underlying pathogenesis of Parkinson's disease (PD), such as apoptosis, calcium homeostasis, and DNA insults.
Insights
Oxidative stress contributes to neurodegeneration. This study identified three proteins—sorcin, annexin V, and ribosomal protein P0—that increase during 1-methyl-4-phenyl-pyridinium ion (MPP+)-induced apoptosis, suggesting their role in Parkinson's disease pathogenesis.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Oxidative stress is implicated in neurodegenerative diseases.
- The specific proteins responding to oxidative stress in neuronal injury are not fully understood.
- Parkinson's disease (PD) involves dopaminergic neurodegeneration, potentially linked to oxidative stress.
Purpose of the Study:
- To identify proteins altered in response to oxidative stress-induced neuronal injury.
- To investigate the role of specific proteins in 1-methyl-4-phenyl-pyridinium ion (MPP+)-induced apoptosis.
- To explore potential mechanisms in Parkinson's disease pathogenesis.
Main Methods:
- Utilized SH-SY5Y cells treated with the neurotoxin 1-methyl-4-phenyl-pyridinium ion (MPP+) to model neuronal injury.
- Employed 2D-Difference Gel Electrophoresis (2D-DIGE) to separate and quantify protein changes.
- Applied Matrix-Assisted Laser Desorption/Ionization-Time of Flight Mass Spectrometry (MALDI-TOF-MS) for protein identification.
Main Results:
- Proteomics analysis identified 22 differentially expressed proteins in MPP+-treated cells (7 up-regulated, 15 down-regulated).
- Sorcin, annexin V, and ribosomal protein P0 were significantly up-regulated.
- Increased levels of these three proteins suggest a role in MPP+-induced apoptosis.
Conclusions:
- Sorcin, annexin V, and ribosomal protein P0 are involved in MPP+-induced neuronal apoptosis.
- These findings highlight multifaceted mechanisms in Parkinson's disease, including apoptosis, calcium homeostasis, and DNA damage.
- Further research into these proteins may reveal novel therapeutic targets for Parkinson's disease.
