111 73

Full metadata record

DC FieldValueLanguage
dc.contributor.author한명훈-
dc.date.accessioned2020-09-21T07:23:44Z-
dc.date.available2020-09-21T07:23:44Z-
dc.date.issued2019-10-
dc.identifier.citationSCIENTIFIC REPORTS, v. 9, article no. 15717en_US
dc.identifier.issn2045-2322-
dc.identifier.urihttps://www.nature.com/articles/s41598-019-52083-y-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/154037-
dc.description.abstractAmlodipine, 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.sponsorshipThis 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.isoenen_US
dc.publisherNATURE PUBLISHING GROUPen_US
dc.subjectNEURONAL CELL-DEATHen_US
dc.subjectPERMEABILITY TRANSITIONen_US
dc.subjectOXIDATIVE STRESSen_US
dc.subjectCHANNEL BLOCKERen_US
dc.subjectREGULATORSen_US
dc.subjectISCHEMIAen_US
dc.subjectRECOVERYen_US
dc.subjectBESYLATEen_US
dc.subjectCA2+en_US
dc.titleMitochondria damaged by Oxygen Glucose Deprivation can be Restored through Activation of the PI3K/Akt Pathway and Inhibition of Calcium Influx by Amlodipine Camsylateen_US
dc.typeArticleen_US
dc.relation.volume9-
dc.identifier.doi10.1038/s41598-019-52083-y-
dc.relation.page0-0-
dc.relation.journalSCIENTIFIC REPORTS-
dc.contributor.googleauthorPark, Hyun-Hee-
dc.contributor.googleauthorHan, Myung-Hoon-
dc.contributor.googleauthorChoi, Hojin-
dc.contributor.googleauthorLee, Young Joo-
dc.contributor.googleauthorKim, Jae Min-
dc.contributor.googleauthorCheong, Jin Hwan-
dc.contributor.googleauthorRyu, Je Il-
dc.contributor.googleauthorLee, Kyu-Yong-
dc.contributor.googleauthorKoh, Seong-Ho-
dc.relation.code2019002548-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF MEDICINE[S]-
dc.sector.departmentDEPARTMENT OF MEDICINE-
dc.identifier.pidgksmh80-
dc.identifier.orcidhttps://orcid.org/0000-0003-1728-5017-


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE