Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 고성호 | - |
dc.date.accessioned | 2018-03-09T05:16:48Z | - |
dc.date.available | 2018-03-09T05:16:48Z | - |
dc.date.issued | 2013-04 | - |
dc.identifier.citation | Stem Cells and Development, April 2013, 22(15), P.2112-2120 | en_US |
dc.identifier.issn | 1547-3287 | - |
dc.identifier.uri | http://online.liebertpub.com/doi/abs/10.1089/scd.2012.0604 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/44151 | - |
dc.description.abstract | Neurogenesis in the adult brain is important for memory and learning, and the alterations in neural stem cells (NSCs) may be an important part of Alzheimer's disease pathogenesis. The phosphatidylinositol 3-kinase (PI3K) pathway has been suggested to play an important role in neuronal cell survival and is highly involved in adult neurogenesis. Recently, coenzyme Q10 (CoQ10) was found to affect the PI3K pathway. We investigated whether CoQ10 could restore amyloid beta (A beta)(25-35) oligomer-inhibited proliferation of NSCs by focusing on the PI3K pathway. To evaluate the effects of CoQ10 on A beta(25-35) oligomer-inhibited proliferation of NSCs, NSCs were treated with several concentrations of CoQ10 and/or A beta(25-35) oligomers. BrdU labeling, Colony Formation Assays, and immunoreactivity of Ki-67, a marker of proliferative activity, showed that NSC proliferation decreased with A beta(25-35) oligomer treatment, but combined treatment with CoQ10 restored it. Western blotting showed that CoQ10 treatment increased the expression levels of p85 alpha PI3K, phosphorylated Akt (Ser473), phosphorylated glycogen synthase kinase-3 beta (Ser9), and heat shock transcription factor, which are proteins related to the PI3K pathway in A beta(25-35) oligomers-treated NSCs. To confirm a direct role for the PI3K pathway in CoQ10-induced restoration of proliferation of NSCs inhibited by A beta(25-35) oligomers, NSCs were pretreated with a PI3K inhibitor, LY294002; the effects of CoQ10 on the proliferation of NSCs inhibited by A beta(25-35) oligomers were almost completely blocked. Together, these results suggest that CoQ10 restores A beta(25-35) oligomer-inhibited proliferation of NSCs by activating the PI3K pathway. | en_US |
dc.description.sponsorship | This work was supported by the NanoBio R&D Program of the Korea Science and Engineering Foundation, funded by the Ministry of Education, Science and Technology (2007-04717) and by the National Research Foundation of Korea (NRF) (2010-0009588). | en_US |
dc.language.iso | en | en_US |
dc.publisher | Mary Ann Liebert | en_US |
dc.subject | SYNTHASE KINASE 3-BETA | en_US |
dc.subject | ALZHEIMERS-DISEASE | en_US |
dc.subject | INDUCED NEUROTOXICITY | en_US |
dc.subject | SUBVENTRICULAR ZONE | en_US |
dc.subject | NEUROGENESIS | en_US |
dc.subject | PERSPECTIVE | en_US |
dc.subject | MEMORY | en_US |
dc.subject | MODEL | en_US |
dc.subject | MICE | en_US |
dc.subject | AGE | en_US |
dc.title | Coenzyme Q10 Restores Amyloid Beta-Inhibited Proliferation of Neural Stem Cells by Activating the PI3K Pathway | en_US |
dc.type | Article | en_US |
dc.relation.no | 15 | - |
dc.relation.volume | 22 | - |
dc.identifier.doi | 10.1089/scd.2012.0604 | - |
dc.relation.page | 2112-2120 | - |
dc.relation.journal | STEM CELLS AND DEVELOPMENT | - |
dc.contributor.googleauthor | Choi, H. | - |
dc.contributor.googleauthor | Park, H.-H. | - |
dc.contributor.googleauthor | Lee, K.-Y. | - |
dc.contributor.googleauthor | Choi, N.-Y. | - |
dc.contributor.googleauthor | Lee, Y.-J. | - |
dc.contributor.googleauthor | Koh, S.-H. | - |
dc.contributor.googleauthor | Yu, H.-J. | - |
dc.contributor.googleauthor | Park, J. | - |
dc.contributor.googleauthor | Huh, Y.-M. | - |
dc.contributor.googleauthor | Lee, S.-H. | - |
dc.relation.code | 2013012098 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | ksh213 | - |
dc.identifier.researcherID | 55724367200 | - |
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