Pulsed Electromagnetic Fields Stimulate HIF-1α-Independent VEGF Release in 1321N1 Human Astrocytes Protecting Neuron-Like SH-SY5Y Cells from Oxygen-Glucose Deprivation.
Astrocytes
/ cytology
Cell Hypoxia
Cell Survival
Cells, Cultured
Electromagnetic Fields
Gene Expression Regulation
Glucose
/ deficiency
Humans
Hypoxia-Inducible Factor 1, alpha Subunit
/ genetics
Neuroblastoma
/ etiology
Oxygen
/ metabolism
Protective Agents
Signal Transduction
Vascular Endothelial Growth Factor A
/ genetics
VEGF
astrocyte-conditioned medium
astrocytes
pulsed electromagnetic fields
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
28 Oct 2020
28 Oct 2020
Historique:
received:
16
09
2020
revised:
26
10
2020
accepted:
28
10
2020
entrez:
31
10
2020
pubmed:
1
11
2020
medline:
26
3
2021
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 33126773
pii: ijms21218053
doi: 10.3390/ijms21218053
pmc: PMC7663527
pii:
doi:
Substances chimiques
HIF1A protein, human
0
Hypoxia-Inducible Factor 1, alpha Subunit
0
Protective Agents
0
VEGFA protein, human
0
Vascular Endothelial Growth Factor A
0
Glucose
IY9XDZ35W2
Oxygen
S88TT14065
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
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