scholarly journals Comparative mRNA Expression of eEF1A Isoforms and a PI3K/Akt/mTOR Pathway in a Cellular Model of Parkinson’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Kawinthra Khwanraj ◽  
Suriyat Madlah ◽  
Khwanthana Grataitong ◽  
Permphan Dharmasaroja
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mrna Level ◽  
Elongation Factor ◽  
Relative Increase ◽  
Mtor Pathway ◽  
Gene Profiling ◽  
Cellular Model ◽  
Protein Elongation

The PI3K/Akt/mTOR pathway is one of dysregulated pathways in Parkinson’s disease (PD). Previous studies in nonneuronal cells showed that Akt regulation can be increased by eukaryotic protein elongation factor 1 alpha 2 (eEF1A2). eEF1A2 is proposed to contribute protection against apoptotic death, likely through activation of the PI3K/Akt pathway. Whether eEF1A2 plays a role in the prevention of cell death in PD has not been investigated. Recently, gene profiling on dopaminergic neurons from postmortem PD patients showed both upregulation and downregulation of some PI3K and mTOR genes. In this paper, the expression of all gene members of the PI3K/Akt/mTOR pathway in relation to those of the eEF1A isoforms in a cellular model of PD was investigated at the mRNA level. The results showed a similar trend of upregulation of genes of the eEF1A isoforms (eEF1A1andeEF1A2) and of the PI3K (classes I–III)/Akt (Akt1,Akt2, andAkt3)/mTOR (mTORC1andmTORC2) pathway in both nondifferentiated and differentiated SH-SY5Y dopaminergic cells treated with 1-methyl-4-phenylpyridinium (MPP+). Upregulation ofeEF1A2,Akt1, andmTORC1was consistent with the relative increase of eEF1A2, Akt, phospho-Akt, and mTORC1 proteins. The possible role of eEF1A isoforms in the regulation of the PI3K/Akt/mTOR pathway in PD is discussed.

scholarly journals Role of ubiquitin ligase HRD1 in a cellular model of Parkinson's disease

2018 ◽  
Vol WCP2018 (0) ◽  
pp. PO4-1-140
Author(s):  
Tomohiro Omura ◽  
Hiroki Matsuda ◽  
Luna Nomura ◽  
Masato Naito ◽  
Shunsaku Nakagawa ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Ubiquitin Ligase ◽  
Cellular Model

scholarly journals Anti-Apoptotic and Anti-Inflammatory Role of Trans ε-Viniferin in a Neuron–Glia Co-Culture Cellular Model of Parkinson’s Disease

Foods ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 586
Author(s):  
Domenico Sergi ◽  
Alex Gélinas ◽  
Jimmy Beaulieu ◽  
Justine Renaud ◽  
Emilie Tardif-Pellerin ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nerve Growth Factor ◽  
Culture System ◽  
Cellular Model ◽  
Dopaminergic Cells ◽  
Inflammatory Molecule ◽  
Anti Inflammatory ◽  
6 Hydroxydopamine

The polyphenol trans-ε-viniferin (viniferin) is a dimer of resveratrol, reported to hold antioxidant and anti-inflammatory properties. The aims of our study were to evaluate the neuroprotective potential of viniferin in the nerve growth factor (NGF)-differentiated PC12 cells, a dopaminergic cellular model of Parkinson’s disease (PD) and assess its anti-inflammatory properties in a N9 microglia–neuronal PC12 cell co-culture system. The neuronal cells were pre-treated with viniferin, resveratrol or their mixture before the administration of 6-hydroxydopamine (6-OHDA), recognized to induce parkinsonism in rats. Furthermore, N9 microglia cells, in a co-culture system with neuronal PC12, were pre-treated with viniferin, resveratrol or their mixture to investigate whether these polyphenols could reduce lipopolysaccharide (LPS)-induced inflammation. Our results show that viniferin as well as a mixture of viniferin and resveratrol protects neuronal dopaminergic cells from 6-OHDA-induced cytotoxicity and apoptosis. Furthermore, when viniferin, resveratrol or their mixture was used to pre-treat microglia cells in our co-culture system, they reduced neuronal cytotoxicity induced by glial activation. Altogether, our data highlight a novel role for viniferin as a neuroprotective and anti-inflammatory molecule in a dopaminergic cellular model, paving the way for nutraceutical therapeutic avenues in the complementary treatments of PD.

scholarly journals Kinin Peptides Enhance Inflammatory and Oxidative Responses Promoting Apoptosis in a Parkinson’s Disease Cellular Model

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Anna Niewiarowska-Sendo ◽  
Andrzej Kozik ◽  
Ibeth Guevara-Lora
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Receptor Expression ◽  
Cellular Model ◽  
Enhanced Production ◽  
Kinin Receptors ◽  
Kinin Receptor ◽  
Inflammatory Processes

Kinin peptides ubiquitously occur in nervous tissue and participate in inflammatory processes associated with distinct neurological disorders. These substances have also been demonstrated to promote the oxidative stress. On the other hand, the importance of oxidative stress and inflammation has been emphasized in disorders that involve the neurodegenerative processes such as Parkinson’s disease (PD). A growing number of reports have demonstrated the increased expression of kinin receptors in neurodegenerative diseases. In this study, the effect of bradykinin and des-Arg10-kallidin, two representative kinin peptides, was analyzed with respect to inflammatory response and induction of oxidative stress in a PD cellular model, obtained after stimulation of differentiated SK-N-SH cells with a neurotoxin, 1-methyl-4-phenylpyridinium. Kinin peptides caused an increased cytokine release and enhanced production of reactive oxygen species and NO by cells. These changes were accompanied by a loss of cell viability and a greater activation of caspases involved in apoptosis progression. Moreover, the neurotoxin and kinin peptides altered the dopamine receptor 2 expression. Kinin receptor expression was also changed by the neurotoxin. These results suggest a mediatory role of kinin peptides in the development of neurodegeneration and may offer new possibilities for its regulation by using specific antagonists of kinin receptors.

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