Lack of the P2X₇ receptor protects against AMD-like defects and microparticle accumulation in a chronic oxidative stress-induced mouse model of AMD.

ABSTRACT: The P2X₇ receptor (P2X₇R) is an ATP-gated ion channel that is a key player in oxidative stress under pathological conditions. The P2X₇R is expressed in the retinal pigmented epithelium (RPE) and neural retina. Chronic oxidative stress contributes to the pathogenesis of age-related macular degeneration (AMD). Mice lacking Cu, Zn superoxide dismutase (Sod1) developed chronic oxidative stress as well as AMD-like features, but whether the P2X₇R plays a causative role in oxidative stress-induced AMD is unknown. Thus, the main purpose of this study was to test if concurrent knockout (KO) of P2X₇R could block AMD-like defects seen in Sod1 KO mice. Using multiple approaches, we demonstrate that Sod1 KO causes AMD-like defects, including positi

SUBMITTER: Carver KA 

PROVIDER: S-EPMC5195873 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature