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Electromagnetic field (10 Hz, 1 mT) protects mesenchymal stem cells from oxygen-glucose deprivation-induced cell death by reducing intracellular Ca2+ and reactive oxygen species

Authors
Jung, Jong HyeokKim, Jae Young
Issue Date
May-2017
Publisher
UNIV SOUTH BOHEMIA
Keywords
Ca2+; Electromagnetic fields; Mesenchymal stem cell; Oxygen and glucose deprivation; Reactive oxygen species
Citation
JOURNAL OF APPLIED BIOMEDICINE, v.15, no.2, pp.112 - 118
Journal Title
JOURNAL OF APPLIED BIOMEDICINE
Volume
15
Number
2
Start Page
112
End Page
118
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/6198
DOI
10.1016/j.jab.2016.11.003
ISSN
1214-021X
Abstract
Protective effects of electromagnetic fields (EMFs) against oxygen and glucose deprivation (OGD)induced human mesenchymal stem cell (MSC) death were studied. Cell survival, intracellular calcium and ROS/RNS levels were measured after culturing MSCs for 3 h under OGD with or without EMF exposure. The survival rate of cells cultured under OGD condition was significantly reduced compared to control cells, while cells cultured in OGD with 10 Hz/1 mT EMF exposure had higher survival ratio than that in equivalent non-exposed cells. This protective effect of EMF was not observed at different frequency/intensity combinations such as 10 Hz/0.01 mT, 10 Hz/0.1 mT, 50 Hz/1 mT and 100 Hz/1 mT. ROS/ RNS levels of cells cultured under OGD conditions significantly increased compared to the control level while 10 Hz/1 mT EMF alleviated this effect. Intracellular calcium levels in OGD group were higher than control while those in OGD plus 10 Hz/1 mT EMF group were significantly lower than OGD group. Addition of Ca2+ chelator promoted protective effects of EMF against OGD-induced MSC death. Our results suggest that 10 Hz/1 mT EMF exposure protects MSCs from OGD-induced cell death and the underlying mechanisms of the protection are reduction of intracellular levels of Ca2+ and ROS/RNS. (C) 2016 Faculty of Health and Social Sciences, University of South Bohemia in Ceske Budejovice. Published by Elsevier Sp. z o. o. All rights reserved.
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