Hydrogen peroxide decreases the survival rate of HeLa cells with stable knockdown of survival motor neuron protein

The mutations of survival motor neuron (SMN) gene result in spinal muscular atrophy (SMA), a common neurodegenerative disease. Some of the motor neurons undergoing cell death is the predominant characteristic in SMA pathology. However, the viability and sensitivity to stresses of other cell types al...

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Main Authors: Ting-Yuan Liu, Chung-Yee Yuo, Cheng-Hsing Kao, Chao-Neng Tseng, Yuh-Jyh Jong, Jan-Gowth Chang, Shou-Mei Wu, Yung-Fu Chang, 劉鼎元, 游仲逸, 高振興, 曾昭能, 鐘育志, 張建國, 吳秀梅, 張永福
Format: Article
Language:English
Published: Wiley 2011-03-01
Series:Kaohsiung Journal of Medical Sciences
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Online Access:http://www.sciencedirect.com/science/article/pii/S1607551X10000355
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Summary:The mutations of survival motor neuron (SMN) gene result in spinal muscular atrophy (SMA), a common neurodegenerative disease. Some of the motor neurons undergoing cell death is the predominant characteristic in SMA pathology. However, the viability and sensitivity to stresses of other cell types also need to be determined. In this article, we established HeLa stable cell line with inducible SMN knockdown to study its viability and sensitivity to oxidative stress. SMN knockdown in the HeLa stable cell line was induced by doxycycline. The proliferative and survival rates of SMN knockdown cells with or without hydrogen peroxide (H2O2) treatment were determined. Our results showed that the proliferative rate of SMN knockdown cells decreased only slightly compared with that of the cells without doxycycline treatment. In contrast, after H2O2 reached certain concentrations, the survival rate of SMN knockdown cells decreased significantly. Our data indicate that SMN knockdown alone is not critical to cell viability. However, when SMN knockdown cells are under stress, such as oxidative stress, their survival rate may significantly decrease. Our results will be helpful to prevent the detrimental effect caused by the cell death of non-motor neurons under stress in SMA patients. In addition, the cell model we established can be used to study the mechanism and screen drugs to prevent the detrimental effects in cases of SMA disease.
ISSN:1607-551X