arginase 2 deletion reduces neuro-glial injury and improves retinal function in a model of retinopathy of prematurity精氨酸酶2删除降低neuro-glial损伤和改善视网膜功能模型中早熟的视网膜病变.pdfVIP

Arginase 2 Deletion Reduces Neuro-Glial Injury and Improves Retinal Function in a Model of Retinopathy of Prematurity 1,2 1 3 1 3 Subhadra P. Narayanan , Jutamas Suwanpradid , Alan Saul , Zhimin Xu , Amber Still , Robert W. Caldwell4, Ruth B. Caldwell1,2,3,5* 1Vascular Biology Center, Georgia Health Sciences University, Augusta, Georgia, United States of America, 2 Department of Cellular Biology and Anatomy, Georgia Health Sciences University, Augusta, Georgia, United States of America, 3 Department of Ophthalmology, Georgia Health Sciences University, Augusta, Georgia, United States of America, 4 Department of Pharmacology and Toxicology, Georgia Health Sciences University, Augusta, Georgia, United States of America, 5 Charlie Norwood VA Medical Center, Augusta, Georgia, United States of America Abstract Background: Retinopathy of prematurity (ROP) is a major cause of vision impairment in low birth weight infants. While previous work has focused on defining the mechanisms of vascular injury leading to retinal neovascularization, recent studies show that neurons are also affected. This study was undertaken to determine the role of the mitochondrial arginine/ ornithine regulating enzyme arginase 2 (A2) in retinal neuro-glial cell injury in the mouse model of ROP. Methods and Findings: Studies were performed using wild type (WT) and A2 knockout (A22/ 2) mice exposed to Oxygen Induced Retinopathy (OIR). Neuronal injury and apoptosis were assessed using immunohistochemistry, TUNEL (terminal deoxynucleotidyl transferase dUTP nick end) labeling and Western blotting. Electroretinography (ERG) was used to assess retinal function. Neuro-glial injury in WT ROP mice was evident by TUNEL labeling, retinal thinning, decreases