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Sébastien Jean Méthot, Sébastien P Gendron, Mathieu Theriault, Stephanie Proulx, Patrick J Rochette; Implication of oxidation and mitochondrial alterations in Fuchs endothelial corneal dystrophy. Invest. Ophthalmol. Vis. Sci. 2017;58(8):1442.
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© ARVO (1962-2015); The Authors (2016-present)
The exact aetiology of the Fuchs endothelial corneal dystrophy (FECD) is not well determined but evidence clearly shows that oxidative stress is a contributing factor. Previous work in our lab has shown that endothelial cells from FECD patients have shorter telomeres and higher mitochondrial levels, indicators of an oxidative stress. We have also shown that FECD cells are not equally affected, with a sub population of cells presenting a normal mitochondrial level. We hypothesised that, due to mitochondrial dysfunction, mitochondrial transmembrane potential (ΔΨ) is reduced in FECD cells, but not all cells are equally affected.
JC-1 dye has been used to measure ΔΨ on corneal endothelial explants and cultured cells form healthy and FECD patients. Mitotracker has been used to control for previously observed difference in mitochondria level. JC-1 and Mitotracker fluorescence intensities have been quantified in individual cell.
ΔΨ is generally lower in endothelial explants from FECD patients when compared to healthy individuals. However, ΔΨ is unevenly distributed in FECD explants. Indeed, 3 distinct cell populations can be described: one with high level of mitochondria and high ΔΨ, one with high level of mitochondria and medium ΔΨ and one with low level of mitochondria and low ΔΨ. When endothelial FECD cells are cultured in vitro, the ΔΨ returns to a level comparable to healthy cells.
FECD corneal endothelial cells have a reduced ΔΨ possibly due to oxidative stress causing mitochondrial alteration, which would lead to the opening of mitochondrial permeability transition pores.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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