Abstract
Pulsed electromagnetic fields (PEMFs) are emerging as an innovative, non-invasive therapeutic option in different pathological conditions of the central nervous system, including cerebral ischemia. This study aimed to investigate the mechanism of action of PEMFs in an in vitro model of human astrocytes, which play a key role in the events that occur following ischemia. 1321N1 cells were exposed to PEMFs or hypoxic conditions and the release of relevant neurotrophic and angiogenic factors, such as VEGF, EPO, and TGF-β1, was evaluated by means of ELISA or AlphaLISA assays. The involvement of the transcription factor HIF-1α was studied by using the specific inhibitor chetomin and its expression was measured by flow cytometry. PEMF exposure induced a time-dependent, HIF-1α-independent release of VEGF from 1321N1 cells. Astrocyte conditioned medium derived from PEMF-exposed astrocytes significantly reduced the oxygen-glucose deprivation-induced cell proliferation and viability decrease in the neuron-like cells SH-SY5Y. These findings contribute to our understanding of PEMFs action in neuropathological conditions and further corroborate their therapeutic potential in cerebral ischemia.
Highlights
Biophysical stimulation employing pulsed electromagnetic fields (PEMFs) is widely used in orthopedic practice to promote bone healing and joint chondroprotection [1]
The effect of PEMFs was investigated on the production of vascular endothelial growth factor (VEGF), EPO and TGFβ1, well-known neurotrophic and neuroprotective factors released from glial cells in response to hypoxic, excitotoxic, or metabolic injury
In 1321N1 cells, used as a model of astrocytes, exposure to PEMFs promoted the release of VEGF, an angiogenic factor with neuroprotective and neurotrophic effects
Summary
Biophysical stimulation employing pulsed electromagnetic fields (PEMFs) is widely used in orthopedic practice to promote bone healing and joint chondroprotection [1]. In a rabbit model of transient focal ischemia, PEMF exposure attenuated cortical ischemia edema and reduced ischemic neuronal damage [6]. In mice subjected to photothrombotic occlusion, PEMFs increased pro-survival proteins, while decreased pro-apoptotic proteins and pro-inflammatory mediators activating the BDNF/TrkB/Akt signaling pathway [8]. We reported the protective effect of PEMFs on hypoxia and inflammation damage in neuron-like and microglial cells [9]. We investigated the signaling pathway that underlies the anti-apoptotic and pro-survival effect of PEMFs in neuron-like cells subjected to hypoxia through the activation of p38 kinase cascade enrolling HSP70, CREB, BDNF, and regulating the Bcl-2 family proteins [10] and the anti-inflammatory effect of PEMFs in microglial cells [11]
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