Endothelial arginase 2 mediates retinal ischemia/reperfusion injury by inducing mitochondrial dysfunction.

ABSTRACT:

Objective

Retinal ischemic disease is a major cause of vision loss. Current treatment options are limited to late-stage diseases, and the molecular mechanisms of the initial insult are not fully understood. We have previously shown that the deletion of the mitochondrial arginase isoform, arginase 2 (A2), limits neurovascular injury in models of ischemic retinopathy. Here, we investigated the involvement of A2-mediated alterations in mitochondrial dynamics and function in the pathology.

Methods

We used wild-type (WT), global A2 knockout (A2KO-) mice, cell-specific A2 knockout mice subjected to retinal ischemia/reperfusion (I/R), and bovine retinal endothelial cells (BRECs) subjected to an oxygen-glucose deprivation/reperfusion (OGD/R) insult. We used western blotting to measu

SUBMITTER: Shosha E 

PROVIDER: S-EPMC8274341 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature