scholarly journals Microarray analysis of oxidative stress regulated genes in mesencephalic dopaminergic neuronal cells: Relevance to oxidative damage in Parkinson's disease

2007 ◽  
Vol 50 (6) ◽  
pp. 834-847 ◽  
Author(s):  
V ANANTHARAM ◽  
E LEHRMANN ◽  
A KANTHASAMY ◽  
Y YANG ◽  
P BANERJEE ◽  
...  
2003 ◽  
Vol 110 (1) ◽  
pp. 76-84 ◽  
Author(s):  
Myung S Yoo ◽  
Hong S Chun ◽  
Jessica J Son ◽  
Lorraine A DeGiorgio ◽  
Dae J Kim ◽  
...  

RSC Advances ◽  
2016 ◽  
Vol 6 (111) ◽  
pp. 110040-110046 ◽  
Author(s):  
Seon-Heui Cha ◽  
Soo-Jin Heo ◽  
You-Jin Jeon ◽  
Sang Myun Park

Dopaminergic neurons are particularly vulnerable to oxidative stress, which may initiate a cascade of intracellular toxic events that lead to protein aggregation and subsequent cell death, causing Parkinson's disease.


2017 ◽  
Vol 2017 ◽  
pp. 1-9
Author(s):  
Yihui Xu ◽  
Wei Lin ◽  
Shuifen Ye ◽  
Huajin Wang ◽  
Tingting Wang ◽  
...  

Oxidative damage plays a critical role in the etiology of neurodegenerative disorders including Parkinson’s disease (PD). In our study, an ancient Chinese kidney-tonifying formula, which consists ofCistanche,Epimedii,andPolygonatum cirrhifolium, was investigated to protect MES23.5 dopaminergic neurons against hydrogen peroxide- (H2O2-) induced oxidative damage. The damage effects of H2O2on MES23.5 cells and the protective effects of KTF against oxidative stress were evaluated using MTT assay, transmission electron microscopy (TEM), immunocytochemistry (ICC), enzyme-linked immunosorbent assay (ELISA), and immunoblotting. The results showed that cell viability was dramatically decreased after a 12 h exposure to 150 μM H2O2. TEM observation found that the H2O2-treated MES23.5 cells presented cellular organelle damage. However, when cells were incubated with KTF (3.125, 6.25, and 12.5 μg/ml) for 24 h after H2O2exposure, a significant protective effect against H2O2-induced damage was observed in MES23.5 cells. Using ICC, we found that KTF inhibited the reduction of the tyrosine hydroxylase (TH) induced by H2O2, upregulated the mRNA and protein expression of HO-1, CAT, and GPx-1, and downregulated the expression of caspase 3. These results indicated that KTF may provide neuron protection against H2O2-induced cell damage through ameliorating oxidative stress, and our findings provide a new potential strategy for the prevention and treatment of Parkinson’s disease.


2014 ◽  
Vol 206 (5) ◽  
pp. 655-670 ◽  
Author(s):  
Ghazaleh Ashrafi ◽  
Julia S. Schlehe ◽  
Matthew J. LaVoie ◽  
Thomas L. Schwarz

To minimize oxidative damage to the cell, malfunctioning mitochondria need to be removed by mitophagy. In neuronal axons, mitochondrial damage may occur in distal regions, far from the soma where most lysosomal degradation is thought to occur. In this paper, we report that PINK1 and Parkin, two Parkinson’s disease–associated proteins, mediate local mitophagy of dysfunctional mitochondria in neuronal axons. To reduce cytotoxicity and mimic physiological levels of mitochondrial damage, we selectively damaged a subset of mitochondria in hippocampal axons. Parkin was rapidly recruited to damaged mitochondria in axons followed by formation of LC3-positive autophagosomes and LAMP1-positive lysosomes. In PINK1−/− axons, damaged mitochondria did not accumulate Parkin and failed to be engulfed in autophagosomes. Similarly, initiation of mitophagy was blocked in Parkin−/− axons. Our findings demonstrate that the PINK1–Parkin-mediated pathway is required for local mitophagy in distal axons in response to focal damage. Local mitophagy likely provides rapid neuroprotection against oxidative stress without a requirement for retrograde transport to the soma.


2012 ◽  
Vol 11 (4) ◽  
pp. 430-438 ◽  
Author(s):  
Marcella Reale ◽  
Mirko Pesce ◽  
Medha Priyadarshini ◽  
Mohammad A Kamal ◽  
Antonia Patruno

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Manisha Singh ◽  
Manish Jain ◽  
Samrat Bose ◽  
Ashutosh Halder ◽  
Tapas Chandra Nag ◽  
...  

AbstractOxysterols play vital roles in the human body, ranging from cell cycle regulation and progression to dopaminergic neurogenesis. While naïve human mesenchymal stem cells (hMSCs) have been explored to have neurogenic effect, there is still a grey area to explore their regenerative potential after in vitro differentiation. Hence, in the current study, we have investigated the neurogenic effect of 22(R)-hydroxycholesterol (22-HC) on hMSCs obtained from bone marrow, adipose tissue and dental pulp. Morphological and morphometric analysis revealed physical differentiation of stem cells into neuronal cells. Detailed characterization of differentiated cells affirmed generation of neuronal cells in culture. The percentage of generation of non-DA cells in the culture confirmed selective neurogenic potential of 22-HC. We substantiated the efficacy of these cells in neuro-regeneration by transplanting them into Parkinson’s disease Wistar rat model. MSCs from dental pulp had maximal regenerative effect (with 80.20 ± 1.5% in vitro differentiation efficiency) upon transplantation, as shown by various behavioural examinations and immunohistochemical tests. Subsequential analysis revealed that 22-HC yields a higher percentage of functional DA neurons and has differential effect on various tissue-specific primary human MSCs. 22-HC may be used for treating Parkinson’s disease in future with stem cells.


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