Abstract
BackgroundTo determine whether photobiomodulation (PBM) rescued the disruption of Na+/Ca2+ homeostasis and mitochondrial membrane potential by ouabain; the Na, K-ATPase inhibitor. For PBM in this study, a 660 nm LED array was used at energy densities of 0.78, 1.56, 3.12, 6.24, and 9.36 J/cm2.ResultsHCN-2 neuronal cells treated with ouabain showed loss of cell polarity, disrupted cell morphology, and decreased cell viability, which were improved after PBM treatment. We found that ouabain-induced Na, K-ATPase inhibition promoted activation of downstream signaling through Src, Ras, and mitogen-activated protein kinase (MAPK), which were suppressed after PBM treatment. This provided evidence of Na, K-ATPase α-subunit inactivation and intracellular Ca2+ increase. In response to ouabain, we observed activation of Src and MAPK by Na, K-ATPase, decreased mitochondrial membrane potential, and Na+-dependent Ca2+ increases, which were restored by PBM treatment.ConclusionsThis study demonstrated that Na+/K+ imbalance could be regulated by PBM treatment in neuronal cells, and we suggest that PBM is a potential therapeutic tool for Na, K-ATPase targeted neuronal diseases.
Highlights
To determine whether photobiomodulation (PBM) rescued the disruption of Na+/Ca2+ homeostasis and mitochondrial membrane potential by ouabain; the Na, K-ATPase inhibitor
We provide the evidence that protective effect of PBM on ouabin-induced Na, K-ATPase disruption through Src/Ras/mitogen-activated protein kinase (MAPK) in neuronal cells
Cells The human brain cortical neuron cell line HCN-2 (ATCC CRL-10742) was purchased from ATCC (Manassas, VA, USA) and was maintained in Dulbecco’s Modified Eagle Media (DMEM) supplemented with 4 mM l-glutamine, 4.5 g/L glucose, and 10% fetal bovine serum, which were purchased from Life Technologies (Grand Island, NY, USA)
Summary
To determine whether photobiomodulation (PBM) rescued the disruption of Na+/Ca2+ homeostasis and mitochondrial membrane potential by ouabain; the Na, K-ATPase inhibitor. Neuronal activity can be manipulated through molecular mechanisms at several levels: (1) ion channels, (2) neurotransmitters and their receptors, (3) auxiliary intramembranous or cytoplasmic signal transducing molecules, and (4) neurotransmitter transporters. These molecular mechanisms facilitate their conservation through reaccumulation in the terminal and synaptic vesicles of these molecular entities such as neurotransmitters and neurotransmitter transporters to regulate three major cations; Na+, K+, and C a2+ [1,2,3]. We provide the evidence that protective effect of PBM on ouabin-induced Na, K-ATPase disruption through Src/Ras/MAPK in neuronal cells
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