TY - JOUR
T1 - Pulsed electromagnetic fields promote survival and neuronal differentiation of human BM-MSCs
AU - Urnukhsaikhan, Enerelt
AU - Cho, Hyunjin
AU - Mishig-Ochir, Tsogbadrakh
AU - Seo, Young Kwon
AU - Park, Jung Kueg
N1 - Publisher Copyright:
© 2015 Elsevier Inc.
PY - 2016/4/15
Y1 - 2016/4/15
N2 - Pulsed electromagnetic fields (PEMF) are known to affect biological properties such as differentiation, regulation of transcription factor and cell proliferation. However, the cell-protective effect of PEMF exposure is largely unknown. The aim of this study is to understand the mechanisms underlying PEMF-mediated suppression of apoptosis and promotion of survival, including PEMF-induced neuronal differentiation. Treatment of induced human BM-MSCs with PEMF increased the expression of neural markers such as NF-L, NeuroD1 and Tau. Moreover, treatment of induced human BM-MSCs with PEMF greatly decreased cell death in a dose- and time-dependent manner. There is evidence that Akt and Ras are involved in neuronal survival and protection. Activation of Akt and Ras results in the regulation of survival proteins such as Bad and Bcl-xL. Thus, the Akt/Ras signaling pathway may be a desirable target for enhancing cell survival and treatment of neurological disease. Our analyses indicated that PEMF exposure dramatically increased the activity of Akt, Rsk, Creb, Erk, Bcl-xL and Bad via phosphorylation. PEMF-dependent cell protection was reversed by pretreatment with LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K). Our data suggest that the PI3K/Akt/Bad signaling pathway may be a possible mechanism for the cell-protective effects of PEMF.
AB - Pulsed electromagnetic fields (PEMF) are known to affect biological properties such as differentiation, regulation of transcription factor and cell proliferation. However, the cell-protective effect of PEMF exposure is largely unknown. The aim of this study is to understand the mechanisms underlying PEMF-mediated suppression of apoptosis and promotion of survival, including PEMF-induced neuronal differentiation. Treatment of induced human BM-MSCs with PEMF increased the expression of neural markers such as NF-L, NeuroD1 and Tau. Moreover, treatment of induced human BM-MSCs with PEMF greatly decreased cell death in a dose- and time-dependent manner. There is evidence that Akt and Ras are involved in neuronal survival and protection. Activation of Akt and Ras results in the regulation of survival proteins such as Bad and Bcl-xL. Thus, the Akt/Ras signaling pathway may be a desirable target for enhancing cell survival and treatment of neurological disease. Our analyses indicated that PEMF exposure dramatically increased the activity of Akt, Rsk, Creb, Erk, Bcl-xL and Bad via phosphorylation. PEMF-dependent cell protection was reversed by pretreatment with LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K). Our data suggest that the PI3K/Akt/Bad signaling pathway may be a possible mechanism for the cell-protective effects of PEMF.
KW - Apoptosis
KW - Human BM-MSCs
KW - Neuronal differentiation
KW - PEMF
KW - Survival
UR - http://www.scopus.com/inward/record.url?scp=84960497054&partnerID=8YFLogxK
U2 - 10.1016/j.lfs.2016.02.066
DO - 10.1016/j.lfs.2016.02.066
M3 - Article
C2 - 26898125
AN - SCOPUS:84960497054
SN - 0024-3205
VL - 151
SP - 130
EP - 138
JO - Life Sciences
JF - Life Sciences
ER -