Frataxin overexpression in Muller cells protects retinal ganglion cells in a mouse model of ischemia/reperfusion injury in vivo.

ABSTRACT: Müller cells are critical for retinal function and neuronal survival but can become detrimental in response to retinal ischemia and increased oxidative stress. Elevated oxidative stress increases expression of the mitochondrial enzyme frataxin in the retina, and its overexpression is neuroprotective after ischemia. Whether frataxin expression in Müller cells might improve their function and protect neurons after ischemia is unknown. The aim of this study was to evaluate the effect of frataxin overexpression in Müller cells on neuronal survival after retinal ischemia/reperfusion in the mouse in vivo. Retinal ischemia/reperfusion was induced in mice overexpressing frataxin in Müller cells by transient elevation of intraocular pressure. Retinal ganglion cells survival was determined 14 days a

SUBMITTER: Schultz R 

PROVIDER: S-EPMC5859167 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature