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Neuroprotective modifications in retinal Müller cells due to oxidative stress and energy restriction
Author(s) -
ToftKehler A.K.,
Gurunbaram R.,
Brændstrup C.,
Desler C.,
Rasmussen L.,
Skytt D.,
Kolko M.
Publication year - 2015
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2015.0619
Subject(s) - oxidative stress , neuroprotection , viability assay , glutamate receptor , intracellular , oxidative phosphorylation , biology , mitochondrion , microbiology and biotechnology , chemistry , biochemistry , pharmacology , cell , receptor
Purpose The viability of retinal ganglion cells (RGCs) is essential to maintain the neuronal function of the retina. Müller cells (MCs) are assumed to be vital in neuroprotection of the RGCs. In this study, we evaluated modifications in retinal MCs due to oxidative stress and energy restrictions. Methods The human Müller glial cell line, MIO‐M1, was used in all experiments. Changes in glutamate uptake were evaluated in oxidative stressed and energy restricted MCs. The cell viability was evaluated by LDH and MTT assays. Regulations in gene and protein expression were evaluated by qPCR and western blot. The ATP production was measured as well as the mitochondrial activity. Results Glutamate uptake was significantly in energy‐restricted MCs. Simultaneous energy restriction and oxidative stress significantly decreased glutamate uptake. The mitochondrial activity was reduced after exposure to energy restriction and further reduced during simultaneous exposure to energy restriction and oxidative stress. The intracellular ATP levels were decreased in the latter condition. Conclusions Oxidative stress and energy restriction alter the neuroprotective characteristics of MCs by increasing the glutamate uptake during energy restriction and by decreasing the uptake during simultaneous exposure to energy restriction and oxidative stress. The impaired mitochondrial activity and reduction of intracellular ATP levels may affect the ability of MCs to maintain a ellular homeostasis in such way that their ability to protect RGCs may to suffer.