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Behavioral Assessments of Spontaneous Locomotion in a Murine MPTP-induced Parkinson's Disease Model
Published on: January 7, 2019
Is X-linked methyl-CpG binding protein 2 a new target for the treatment of Parkinson's disease
Teng Xie1, Jie Zhang1, Xianhou Yuan1
1Department of Neurosurgery, Zhongnan Hospital of Wuhan University, Wuhan 430071, Hubei Province, China.
Abstract:
X-linked methyl-CpG binding protein 2 mutations can induce symptoms similar to those of Parkinson's disease and dopamine metabolism disorders, but the specific role of X-linked methyl-CpG binding protein 2 in the pathogenesis of Parkinson's disease remains unknown. In the present study, we used 6-hydroxydopamine-induced human neuroblastoma cell (SH-SY5Y cells) injury as a cell model of Parkinson's disease. The 6-hydroxydopamine (50 μmol/L) treatment decreased protein levels for both X-linked methyl-CpG binding protein 2 and tyrosine hydroxylase in these cells, and led to cell death. However, overexpression of X-linked methyl-CpG binding protein 2 was able to ameliorate the effects of 6-hydroxydopamine, it reduced 6-hydroxydopamine-induced apoptosis, and increased the levels of tyrosine hydroxylase in SH-SY5Y cells. These findings suggesting that X-linked methyl-CpG binding protein 2 may be a potential therapeutic target for the treatment of Parkinson's disease.
Insights
X-linked methyl-CpG binding protein 2 (MECP2) may protect against Parkinson's disease. Overexpressing MECP2 reduced cell death and increased key protein levels in a Parkinson's disease cell model.
Area of Science:
- Neuroscience
- Genetics
- Cell Biology
Background:
- Mutations in X-linked methyl-CpG binding protein 2 (MECP2) can mimic Parkinson's disease symptoms.
- The precise role of MECP2 in Parkinson's disease (PD) pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the role of MECP2 in a cellular model of Parkinson's disease.
- To determine if MECP2 can protect against neurotoxicity relevant to PD.
Main Methods:
- Utilized a 6-hydroxydopamine (6-OHDA) induced injury model in human neuroblastoma SH-SY5Y cells.
- Assessed the impact of 6-OHDA on MECP2 and tyrosine hydroxylase (TH) protein levels.
- Examined the effects of MECP2 overexpression on 6-OHDA-induced cell death and TH levels.
Main Results:
- 6-OHDA treatment reduced MECP2 and TH protein levels and induced cell death in SH-SY5Y cells.
- Overexpression of MECP2 significantly reduced 6-OHDA-induced apoptosis.
- MECP2 overexpression increased TH levels in the presence of 6-OHDA.
Conclusions:
- MECP2 plays a protective role against 6-OHDA-induced neurotoxicity in a cellular PD model.
- MECP2 may be a potential therapeutic target for Parkinson's disease treatment.
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