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Sublethal Doses of Zinc Protect Rat Neural Stem Cells Against Hypoxia Through Activation of the PI3K Pathway

Title
Sublethal Doses of Zinc Protect Rat Neural Stem Cells Against Hypoxia Through Activation of the PI3K Pathway
Author
이규용
Keywords
hypoxia; phosphatidylinositol-3 kinase; zinc; neural stem cells; sublethal dose
Issue Date
2019-06
Publisher
MARY ANN LIEBERT
Citation
STEM CELLS AND DEVELOPMENT, v. 28, NO 12, Page. 769-780
Abstract
Cerebral infarction is one of the major causes of severe morbidity and mortality, and thus, research has focused on developing treatment options for this condition. Zinc (Zn) is an essential element in the central nervous system and has several neuroprotective effects in the brain. In this study, we examined the neuroprotective effects of Zn on neural stem cells (NSCs) exposed to hypoxia. After treatment with several concentrations of Zn, the viability of NSCs under hypoxic conditions was measured by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, Trypan blue staining, and a lactate dehydrogenase assay. To evaluate the effect of Zn on the proliferation of NSCs, bromodeoxyuridine/5-bromo-2′-deoxyuridine (BrdU) labeling and colony formation assays were performed. Apoptosis was also examined in NSCs exposed to hypoxia with and without Zn treatment. In addition, a western blot analysis was performed to evaluate the effect of Zn on intracellular signaling proteins. NSC viability and proliferation were decreased under hypoxic conditions, but treatment with sublethal doses of Zn restored viability and proliferation. Sublethal doses of Zn reduced apoptosis caused by hypoxia, increased the expression levels of proteins related to the phosphatidylinositol-3 kinase (PI3K) pathway, and decreased the expression levels of proteins associated with neuronal cell death. These findings confirm that in vivo, sublethal doses of Zn protect NSCs against hypoxia through the activation of the PI3K pathway. Thus, Zn could be employed as a therapeutic option to protect NSCs in ischemic stroke.
URI
https://www.liebertpub.com/doi/10.1089/scd.2018.0138http://repository.hanyang.ac.kr/handle/20.500.11754/110732
ISSN
1547-3287; 1557-8534
DOI
10.1089/scd.2018.0138
Appears in Collections:
COLLEGE OF MEDICINE[S](의과대학) > MEDICINE(의학과) > Articles
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