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Neuroprotective Effect of Low Frequency-Pulsed Electromagnetic Fields in Ischemic Stroke
Urnukhsaikhan, Enerelt,Mishig-Ochir, Tsogbadrakh,Kim, Soo-Chan,Park, Jung-Keug,Seo, Young-Kwon Humana Press 2017 Applied biochemistry and biotechnology Vol. No.
<P>Low frequency-pulsed electromagnetic fields (LF-PEMFs) affect many biological processes; however, the fundamental mechanisms responsible for these effects remain unclear. Our study aimed to investigate the effect of LF-PEMFs on neuroprotection after ischemic stroke. C57B6 mice were exposed to LF-PEMF (F = 60 Hz, Bm = 10 mT) after photothrombotic occlusion. We measured the BDNF/TrkB/Akt signaling pathway, pro-apoptotic and pro-survival protein and gene expressions, and the expression of inflammatory mediators and performed behavioral tests in both LF-PEMF-treated and untreated ischemic stroke mice. Our results showed that LF-PEMF treatment promotes activation of the BDNF/TrkB/Akt signaling pathway. Subsequently, pro-survival proteins were significantly increased, while pro-apoptotic proteins and inflammatory mediators were decreased in ischemic stroke mice after LF-PEMF treatment. The results demonstrated that LF-PEMF exposure has a neuroprotective effect after ischemic stroke in mice during the recovery process.</P>
Pulsed electromagnetic fields promote survival and neuronal differentiation of human BM-MSCs
Urnukhsaikhan, E.,Cho, H.,Mishig-Ochir, T.,Seo, Y.K.,Park, J.K. Pergamon 2016 Life sciences Vol.151 No.-
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.
Enerelt Urnukhsaikhan 동중앙아시아경상학회 2015 한몽경상학회 학술대회 Vol.2015 No.04
There is cumulative evidence that the Akt and Ras are involved in neuronal survival and protection. The Akt and Ras activates, resulting in the regulation of survival proteins such as BAD and Bcl-xL. Thus, Akt/Ras signaling pathway may be one propitious target for treatment of neurological disease. Pulsed electromagnetic field (PEMF) is known to have effects on 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 underlying mechanisms that PEMF suppressing apoptosis and promoting survival, including PEMF induced neuronal differentiation. In induced human BM-MSCs treated with PEMF, the expression of neural msarkers such as NF-L, NeuroD1 and Tau increased. Moreover, treatment of induced human BM-MSCs with PEMF exposure greatly decreased cell death in the dose and time dependent manner. Additionally, Analysis indicated that PEMF exposure dramatically promoted activities of Akt, Rsk, Creb, Erk, Bcl-xL and Bad phosphorylation. Meanwhile, the PEMF dependent cell protection was notably reversed by pretreatment with LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K). Our data suggest that PI3K/Akt/Bad signalling pathway may be a possible mechanism involved in the cell protective effect of PEMF.
Choi, Yun-Kyong,Urnukhsaikhan, Enerelt,Yoon, Hee-Hoon,Seo, Young-Kwon,Cho, Hyunjin,Jeong, Jong-Seob,Kim, Soo-Chan,Park, Jung-Keug Wiley (John WileySons) 2017 Biotechnology progress Vol.33 No.1
<P>Biophysical wave stimulus has been used as an effective tool to promote cellular maturation and differentiation in the construction of engineered tissue. Pulsed electromagnetic fields (PEMFs) and sound waves have been selected as effective stimuli that can promote neural differentiation. The aim of this study was to investigate the synergistic effect of PEMFs and sound waves on the neural differentiation potential in vitro and in vivo using human bone marrow mesenchymal stem cells (hBM-MSCs). In vitro, neural-related genes in hBM-MSCs were accelerated by the combined exposure to both waves more than by individual exposure to PEMFs or sound waves. The combined wave also up-regulated the expression of neural and synaptic-related proteins in a three-dimensional (3-D) culture system through the phosphorylation of extracellular signal-related kinase. In a mouse model of photochemically induced ischemia, exposure to the combined wave reduced the infarction volume and improved post-injury behavioral activity. These results indicate that a combined stimulus of biophysical waves, PEMFs and sound can enhance and possibly affect the differentiation of MSCs into neural cells. Our study is meaningful for highlighting the potential of combined wave for neurogenic effects and providing new therapeutic approaches for neural cell therapy. (c) 2016 American Institute of Chemical Engineers Biotechnol. Prog., 33:201-211, 2017</P>
Choi, Yun‐,Kyong,Urnukhsaikhan, Enerelt,Yoon, Hee‐,Hoon,Seo, Young‐,Kwon,Park, Jung‐,Keug WILEY 2016 BIOTECHNOLOGY JOURNAL Vol.11 No.11
<P><B>Abstract</B></P><P>Various animal models of stroke have been developed to simulate the human stroke with the development of the ischemic method facilitates preclinical stroke research. The photothrombotic ischemia model, based on the intravascular photochemical reaction, is widely used for in vivo studies. However, this study has limitations, which generated a relatively small‐sized infarction model on superficial cortex compared to that of the MCAO stroke model. In this study, the photothorombosis mouse model is adapted and the optimum conditions for generation of cell death and deficits with high reproducibility is determined. The extent of damage within the cortex was assessed by infarct volume and cellular/behavioral analyses. In this model, the neural cell death and inflammatory responses is detected; moreover, the degree of behavioral impairment is correlated with the brain infarct volume. Further, to enhance the understanding of neural repair, the effect of neural differentiation by transplantation of human bone marrow‐derived mesenchymal stem cells (BM‐MSCs) is analyzed. The authors demonstrated that transplantation of BM‐MSCs promoted the neural differentiation and behavioral performance in their photothrombosis model. Therefore, this research was meaningful to provide a stable animal model of stroke with low variability. Moreover, this model will facilitate development of novel MSC‐based therapeutics for stroke.</P>
Cellular Membrane Composition Requirement by Antimicrobial and Anticancer Peptide GA-K4
Mishig-Ochir, Tsogbadrakh,Gombosuren, Davaadulam,Jigjid, Altanchimeg,Tuguldur, Badamkhatan,Chuluunbaatar, Galbadrakh,Urnukhsaikhan, Enerelt,Pathak, Chinar,Lee, Bong-Jin Bentham Science Publishers 2017 Protein and peptide letters Vol.24 No.3