Volume 93, Issue S255
ABS15-0619
Free Access

Neuroprotective modifications in retinal Müller cells due to oxidative stress and energy restriction

A.K. Toft-Kehler

A.K. Toft-Kehler

Department of Neuroscience and Pharmacology, The Panum Institute, Copenhagen, Denmark

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R. Gurunbaram

R. Gurunbaram

Department of Neuroscience and Pharmacology, The Panum Institute, Copenhagen, Denmark

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C. Brændstrup

C. Brændstrup

Department of Neuroscience and Pharmacology, The Panum Institute, Copenhagen, Denmark

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C. Desler

C. Desler

Department of Cellular and Molecular Medicine, The Panum Institute, Copenhagen, Denmark

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L. Rasmussen

L. Rasmussen

Department of Cellular and Molecular Medicine, The Panum Institute, Copenhagen, Denmark

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D. Skytt

D. Skytt

Department of Neuroscience and Pharmacology, The Panum Institute, Copenhagen, Denmark

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M. Kolko

M. Kolko

Department of Neuroscience and Pharmacology, The Panum Institute, Copenhagen, Denmark

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First published: 23 September 2015

Abstract

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.

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