Evaluation of the role of an antioxidant gene in NSC-34 motor neuron-like cells as a model of a motor neuron disease

• Autorzy: Alrafiah A.R.
• Języki publikacji: EN

Abstrakty

EN

Background: Spinal muscular atrophy is a rare genetic disease, which primarily affects motor neurons and predominantly occurs in children. To date, alternatives for the treatment of the disease have been controversial. Spinal muscular atrophy has a multi-factorial aetiology, with mitochondrial oxidative stress considered as the crucial pathogenic mechanism. To determine the mechanisms underlying the loss of motor neurons, NSC-34 motor neuron-like cells are often used as an in vitro model of spinal muscular atrophy. As plastin 3 (PLS3) has been demonstrated as a modifier of spinal muscular atrophy, the aim of the current study was to evaluate the neuroprotective effect of PLS3 in NSC-34 cells. Materials and methods: Plastin 3 was overexpressed in human embryonic kidney 293T cells and NSC-34 cells via lentiviral transduction. NSC-34 cells transduced with a lentiviral vector carrying the gene for LacZ β-galactosidase served as a control. Oxidative stress was then induced by depriving cells of serum, and the protective effect of PLS3 was assessed using a cellular reactive oxygen species detection assay. Results: While PLS3 was successfully overexpressed in human embryonic kidney 293T cells and NSC-34 cells, upregulation of this protein did not significantly decrease oxidative stress in serum-deprived NSC-34 cells relative to controls. Conclusions: Plastin 3 overexpression in NSC-34 cells did not elicit an antioxidative effect following serum deprivation. (Folia Morphol 2019; 78, 1: 1–9)

• Wydawca: -
• Czasopismo: Folia Morphologica
• Rocznik: 2019
• Tom: 78
• Numer: 1
• Opis fizyczny: p.1-9,fig.,ref.

Twórcy

autor

Alrafiah A.R.

• Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, Jeddah, Saudi Arabia
• Neuroscience Research Unit, King Abdulaziz University, Faculty of Medicine, Branch of Sulaymaniyah, Jeddah, Saudi Arabia

Bibliografia

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Identyfikatory

DOI

10.5603/FM.a2018.0072