Ismail Zaitoun, PhD
Credentials: Assistant Professor, Department of Ophthalmology and Visual Sciences
1300 University Ave
Madison, WI 53706
Ph.D. 2008, University of Wisconsin-Madison, Madison, WI
Postdoctoral position, University of Wisconsin-Madison, Madison, WI
Extremely premature children face many health issues, including a strong risk of vision loss. Retinopathy of prematurity (ROP) is a leading cause of visual impairment and loss in these children, affecting more than half of the 0.72% of babies born in the United States weighing 2.75 lbs or less. ROP is driven by the sensitivity of developing retinal vasculature to changes in oxygen levels in premature newborns, the reason for which remains unknown. The Zaitoun lab has focused on retinopathy of prematurity at the cellular and molecular levels, hoping to treat the root causes of this devastating disease. The lab has zeroed in on a family of proteins called Bcl-2, one of whose members—called Bim—appears to have an important role to play when the developing retinal vasculature receives too much oxygen (hyperoxia), destroying blood vessels, or too little oxygen (ischemia), which causes blood vessels to grow too profusely. Utilizing the oxygen-induced retinopathy (OIR) mouse model to study ROP, Dr. Zaitoun’s group and collaborators demonstrated that deleting Bim globally protected the growing blood vessels from either negative effect. Interestingly, deleting Bim in a targeted way, aiming at individual vascular cell types without global deletion, did not show the same protective effects.
Currently funded by an R01 grant from the NIH, the Zaitoun lab is performing experiments to determine the exact roles played by Bim expression and by another protein, vascular endothelial growth factor (VEGF), in the inner retinal neurons and their impact on hyperoxia-induced vascular damage during oxygen-induced ischemic retinopathy. Figuring out the precise mechanisms of action undertaken by these proteins should allow for targeted therapies to prevent retinopathy of prematurity and its accompanying vision loss.
A second line of research in the lab aims to determine the impact of hypoxic-ischemic insult on retinal vascular integrity and function. A great majority of surviving children with hypoxic-ischemic encephalopathy (HIE) display visual impairments. These impairments are usually associated with injuries to certain parts of the cerebral visual systems. In addition, emerging evidence suggests neuronal damage in the retina following HIE. However, how these changes are brought up in the retina, and whether retinal vascular damage contributes to the compromised vision, remains poorly understood. The studies show a significant defect in retinal vascularization in animals subjected to HIE.