Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이규용 | - |
dc.date.accessioned | 2019-09-27T07:49:41Z | - |
dc.date.available | 2019-09-27T07:49:41Z | - |
dc.date.issued | 2019-06 | - |
dc.identifier.citation | STEM CELLS AND DEVELOPMENT, v. 28, NO 12, Page. 769-780 | en_US |
dc.identifier.issn | 1547-3287 | - |
dc.identifier.issn | 1557-8534 | - |
dc.identifier.uri | https://www.liebertpub.com/doi/10.1089/scd.2018.0138 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/110732 | - |
dc.description.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. | en_US |
dc.description.sponsorship | This research was supported by the Basic Science Research Program of the National Research Foundation of Korea, which is funded by the Ministry of Science, ICT and Future Planning (2018R1A2A2A15023219 and 2018R1C1B5044530), by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant number: HI17C2160 and HI18C1254), and by the Medical Research Center (2017R1A5A2015395). | en_US |
dc.language.iso | en | en_US |
dc.publisher | MARY ANN LIEBERT | en_US |
dc.subject | hypoxia | en_US |
dc.subject | phosphatidylinositol-3 kinase | en_US |
dc.subject | zinc | en_US |
dc.subject | neural stem cells | en_US |
dc.subject | sublethal dose | en_US |
dc.title | Sublethal Doses of Zinc Protect Rat Neural Stem Cells Against Hypoxia Through Activation of the PI3K Pathway | en_US |
dc.type | Article | en_US |
dc.relation.no | 12 | - |
dc.relation.volume | 28 | - |
dc.identifier.doi | 10.1089/scd.2018.0138 | - |
dc.relation.page | 769-780 | - |
dc.relation.journal | STEM CELLS AND DEVELOPMENT | - |
dc.contributor.googleauthor | Choi, Hojin | - |
dc.contributor.googleauthor | Choi, Na-Young | - |
dc.contributor.googleauthor | Park, Hyun-Hee | - |
dc.contributor.googleauthor | Lee, Kyu-Yong | - |
dc.contributor.googleauthor | Lee, Young Joo | - |
dc.contributor.googleauthor | Koh, Seong-Ho | - |
dc.relation.code | 2019001103 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | kylee | - |
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