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Folia Morphol (Warsz). 2018 Aug 14. doi: 10.5603/FM.a2018.0072. [Epub ahead of print]

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

Author information

1
Medical Laboratory Technology Department, Faculty of Applied Medical Sciences , King Abdul Aziz University, P.O Box 80200 Jeddah, 21589 Jeddah, Saudi Arabia. aalrafiah@kau.edu.sa.

Abstract

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 etiology, 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 plastin 3 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 plastin 3 was assessed using a cellular reactive oxygen species detection assay.

RESULTS:

While plastin 3 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.

KEYWORDS:

NSC-34 cells; lentiviral vectors; oxidative stress; plastin 3; spinal muscular atrophy

PMID:
30106460
DOI:
10.5603/FM.a2018.0072
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