Vision Research Lab

Vision Research Laboratory

Director: Priya Narayanan, PhD



The Augusta University Vision Research Laboratory focuses on identifying therapeutic targets for ocular diseases such as diabetic retinopathy, retinopathy of prematurity, and optic neuritis, diseases which share a common feature of neurovascular damage in the retina. Both in vivo and in vitro approaches are employed to investigate the role of arginase/polyamine pathway in retinal neurovascular injury. We have previously shown that arginase, the urea cycle enzyme, regulates neuro-glial injury and retinal function in models of retinal neurodegeneration. Current projects explore the cellular and molecular mechanisms by which retinal arginase signaling and its downstream signaling partner, polyamine oxidase, are involved in neuro-vascular protection during retinal injuries. Experiments using knockout mice, cultured cells, and pharmacological inhibitors in ocular disease models have significant implications in the development of new therapies for vision problems.



Priya Narayanan, PhDPriya Narayanan

Assistant Professor
Department of Occupational Therapy
College of Allied Health Sciences
Augusta University
987 St. Sebastian Way, EC-2332
Augusta, GA 30912



Dr. Priya Narayanan is a biomedical scientist interested in investigating the causes of vision disorders through identifying the mechanisms of retinal neuro-vascular damage to retina. She received her doctoral degree in biochemistry from the National Dairy Research Institute in India and did her postdoctoral training at the Department of Neuroscience at the Cleveland Clinic, where she studied the mechanisms of neuro-glial signals regulating central nervous system myelination. She received subsequent training at the Augusta University Vascular Biology Center in neuro-vascular mechanisms of retinal injury and established an independent program in vision research using models of retinal neuro-vascular injury. She is an active member of the Augusta University Culver Vision Discovery Institute.



Role of arginase signaling in multiple sclerosis associated neuronal injury
Using animal models, this study examines the involvement of arginase and its downstream signaling partners in Retinal Ganglion Cells loss.  Studies have shown that multiple sclerosis patients develop optic neuritis characterized by thinning of nerve fiber layer, loss of RGC, and loss of inner retinal function, resulting in visual dysfunction, one of the most common clinical manifestations of MS. We hypothesize that activation of arginase pathway causes neuronal injury in the MS retina.   Principal Investigator, supported by Augusta University Culver Vision Discovery Institute

Role of neuronal arginase on vascular protection during ischemic retinopathy
A study on the impact of neuronal survival on vascular protection under ischemic conditions in the retina. Our central hypothesis is that during retinal ischemia, arginase activity increases resulting in altered nitric oxide signaling and increased polyamine oxidation, leading to the generation of reactive nitrogen species, hydrogen peroxide, and reactive aldehydes, causing neurodegeneration. This further leads to endothelial cell death either by the release of toxic soluble factors or due to the lack of trophic support from degenerating neurons resulting in vascular injury. Our recent studies have shown Arginase 2 functions to reduce neuronal death during hyperoxia through the regulation of polyamine metabolism.  Principal Investigator, supported by American Heart Association

Cellular mechanisms of retinopathy: Role of arginase
An  investigation into the role of Arg2 in neuronal and capillary degeneration resulting from retinal ischemia/reperfusion injury. Excessive activity of the urea cycle enzyme arginase has been implicated in a variety of cardiovascular and neurodegenerative diseases. Preliminary data from this study show that deletion of arginase 2 or inhibition of arginase activity significantly reduces ganglion cell death in the I/R retina. We are currently focusing on the signaling mechanisms by which arginase blockade mediates neuro-vascular protection during I/R injury.  Co-Investigator, supported by National Eye Institute



Patel C, Narayanan SP, Zhang W, Xu Z, Sukumari-Ramesh S, Dhandapani KM, Caldwell RW, Caldwell RB. "Activation of endothelin system mediates pathological angiogenesis during ischemic retinopathy." American Journal of Pathology 2014. Nov; 184(11):3040-51. PMCID: PMC4215027

Narayanan SP, Xu Z, Putluri N, Sreekumar A, Lemtalsi T, Caldwell RW, Caldwell RB. "Arginase 2 deficiency reduces hyperoxia-mediated retinal neurodegeneration through the regulation of polyamine metabolism." Cell Death Disease 2014 Feb 20; 5:e1075. PMCID: PMC3944241.

S. P. Narayanan, M. Rojas, J. Suwanpradid, H.A. Toque, R. W. Caldwell, R.B. Caldwell. "Arginase in Retinopathy." Progress in Retinal and Eye Research 2013. Sep;36:260-80PMCID: PMC3759622

Yokota H, Narayanan SP, Zhang W, Liu H, Rojas M, Xu Z, Lemtalsi T, Nagaoka T, Yoshida A, Brooks SE, Caldwell RW, Caldwell RB "Neuroprotection from retinal ischemia/reperfusion injury by NOX2 NADPH oxidase deletion." Investigative Ophthalmic Visual Science 2011 52(11):8123-31. PMCID: PMC3208002

Narayanan, SP, Suwanpradid, J, Saul, A, Xu, Z, Caldwell, RW and Caldwell, RB  "Deletion of Arginase 2 reduces neurodegeneration and improves retinal function in a mouse model of oxygen induced retinopathy." PLoS ONE6 2011.(7):e22460. PMCID:PMC3141070