Arginase 2 Deletion Reduces Neuro-Glial Injury and Improves Retinal Function in a Model of Retinopathy of Prematurity 英文参考文献.docVIP
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Arginase 2 Deletion Reduces Neuro-Glial Injury and Improves Retinal Function in a Model of Retinopathy of Prematurity 英文参考文献
Arginase2DeletionReducesNeuro-GlialInjuryand
ImprovesRetinalFunctioninaModelofRetinopathyof
Prematurity
SubhadraP.Narayanan1,2,JutamasSuwanpradid1,AlanSaul3,ZhiminXu1,AmberStill3,RobertW.
Caldwell4,RuthB.Caldwell1,2,3,5*
1VascularBiologyCenter,GeorgiaHealthSciencesUniversity,Augusta,Georgia,UnitedStatesofAmerica,2DepartmentofCellularBiologyandAnatomy,GeorgiaHealth
SciencesUniversity,Augusta,Georgia,UnitedStatesofAmerica,3DepartmentofOphthalmology,GeorgiaHealthSciencesUniversity,Augusta,Georgia,UnitedStatesof
America,4DepartmentofPharmacologyandToxicology,GeorgiaHealthSciencesUniversity,Augusta,Georgia,UnitedStatesofAmerica,5CharlieNorwoodVAMedical
Center,Augusta,Georgia,UnitedStatesofAmerica
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
studiesshowthatneuronsarealsoaffected.Thisstudywasundertakentodeterminetheroleofthemitochondrialarginine/
ornithineregulatingenzymearginase2(A2)inretinalneuro-glialcellinjuryinthemousemodelofROP.
MethodsandFindings:Studieswereperformedusingwildtype(WT)andA2knockout(A22/2)miceexposedtoOxygen
Induced Retinopathy (OIR). Neuronal injury and apoptosis were assessed using immunohistochemistry, TUNEL (terminal
deoxynucleotidyltransferasedUTPnickend)labelingandWesternblotting.Electroretinography(ERG)wasusedtoassess
retinalfunction.Neuro-glialinjuryinWTROPmicewasevidentbyTUNELlabeling,retinalthinning,decreasesinnumberof
rodbipolarcellsandglialcellactivationascomparedwithroomaircontrols.SignificantreductioninnumbersofTUNEL
positive cells, inhibition of retinal thinning, preservation of the rod bipolar cells and prevention of glial activation were
observed in the A22/2 retinas. Retinal function was markedly impaired in the WT OIR mice as shown by decreases in
amplitude of the b-wave of the ERG. This defect was significantly reduced in A22/2 mice.
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