Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 정진환 | - |
dc.date.accessioned | 2020-11-13T06:25:30Z | - |
dc.date.available | 2020-11-13T06:25:30Z | - |
dc.date.issued | 2019-10 | - |
dc.identifier.citation | SCIENTIFIC REPORTS, v. 9, article no. 15717 | en_US |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | https://www.nature.com/articles/s41598-019-52083-y | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/155549 | - |
dc.description.abstract | Amlodipine, a L-type calcium channel blocker, has been reported to have a neuroprotective effect in brain ischemia. Mitochondrial calcium overload leads to apoptosis of cells in neurologic diseases. We evaluated the neuroprotective effects of amlodipine camsylate (AC) on neural stem cells (NSCs) injured by oxygen glucose deprivation (OGD) with a focus on mitochondrial structure and function. NSCs were isolated from rodent embryonic brains. Effects of AC on cell viability, proliferation, level of free radicals, and expression of intracellular signaling proteins were assessed in OGD-injured NSCs. We also investigated the effect of AC on mitochondrial structure in NSCs under OGD by transmission electron microscopy. AC increased the viability and proliferation of NSCs. This beneficial effect of AC was achieved by strong protection of mitochondria. AC markedly enhanced the expression of mitochondrial biogenesis-related proteins and mitochondrial anti-apoptosis proteins. Together, our results indicate that AC protects OGD-injured NSCs by protecting mitochondrial structure and function. The results of the present study provide insight into the mechanisms underlying the protective effects of AC on NSCs. | 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 (2018R1D1A1A09082825, 2018R1A2A2A15023219, and 2018R1D1A1B07047722), by a grant of 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: HI18C1254), and by the Medical Research Center (2017R1A5A2015395). | en_US |
dc.language.iso | en | en_US |
dc.publisher | NATURE PUBLISHING GROUP | en_US |
dc.subject | NEURONAL CELL-DEATH | en_US |
dc.subject | PERMEABILITY TRANSITION | en_US |
dc.subject | OXIDATIVE STRESS | en_US |
dc.subject | CHANNEL BLOCKER | en_US |
dc.subject | REGULATORS | en_US |
dc.subject | ISCHEMIA | en_US |
dc.subject | RECOVERY | en_US |
dc.subject | BESYLATE | en_US |
dc.subject | CA2+ | en_US |
dc.title | Mitochondria damaged by Oxygen Glucose Deprivation can be Restored through Activation of the P13K/Akt pathway and inhibition of Calcium influx by Amlodipine Camsylate | en_US |
dc.type | Article | en_US |
dc.relation.volume | 9 | - |
dc.identifier.doi | 10.1038/s41598-019-52083-y | - |
dc.relation.page | 1-11 | - |
dc.relation.journal | SCIENTIFIC REPORTS | - |
dc.contributor.googleauthor | Park, Hyun-Hee | - |
dc.contributor.googleauthor | Han, Myung-Hoon | - |
dc.contributor.googleauthor | Choi, Hojin | - |
dc.contributor.googleauthor | Lee, Young Joo | - |
dc.contributor.googleauthor | Kim, Jae Min | - |
dc.contributor.googleauthor | Cheong, Jin Hwan | - |
dc.contributor.googleauthor | Ryu, Je Il | - |
dc.contributor.googleauthor | Lee, Kyu-Yong | - |
dc.contributor.googleauthor | Koh, Seong-Ho | - |
dc.relation.code | 2019002548 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | cjh2324 | - |
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