Department of Ophthalmology

Research Photo Gallery

The laboratory of Dr. Zsolt Ablonczy (standing) studies retinal edema, the accumulation of extracellular fluid in the retina attributed to inner blood retina barrier (BRB) leakage. Vascular endothelial growth factor (VEGF) plays an important role in this process. Experimental methods used in the Ablonczy laboratory facilitate definitive measurements of the modulatory effects of VEGF on the retinal pigment epithelium (RPE) in vivo.

Geographic atrophy (GA), a “dry” form of advanced stage age-related macular degeneration (AMD), is characterized by loss of blood vessels in the choroid, retinal pigment epithelium (RPE) and photoreceptors. Dr. Jeffrey Blice (seated, center) is investigating new clinical methods designed to prevent the advance of GA and the related deteriorations in visual function.

Dr. Crouch is part of a research group that investigates lipofuscin, an aging marker in the retinal pigment epithelium (RPE) associated with the development of macular degeneration. The most abundant component of RPE lipofuscin is the bis-retinoid A2E, but its exact composition is unknown. Using MALDI imaging, many known adducts of A2E were identified, providing evidence that mass spectrometric imaging can be utilized as a tool to begin to identify the molecular substructure of clinically-relevant diagnostic information.

Using color fundus photographs and spectral domain optical coherence tomography (SD-OCT), Dr. Lucian V. Del Priore (seated, center) assesses retinal structures such as Bruch’s membrane and retinal pigment epithelium (RPE) for patient eligibility in a pre-clinical study to generate patient-specific induced pluripotent cells (iPSCs). Restoration of vision for patients with advanced retinal degenerations will require transplantation of new RPE into the bed of atrophy. The use of patient-specific iPS-derived RPE is advantageous chiefly because of the avoidance of graft rejection. 

The laboratory of Dr. Shahid Husain (standing, left) performs Western blotting to measure nitrosylation in the retina using nitrotyrosine antibodies in response to glaucomatous injury. Nitric oxide production is one of the mechanisms that lead to retinal ganglion cell (RGC) death in glaucoma. Dr. Husain’s data supports the idea that nitric oxide plays a detrimental role during glaucomatous injury, and its inhibition provides retina neuroprotection against glaucomatous injury.

In age-related macular degeneration (AMD), disease severity is correlated with cell death via the membrane attack complex (MAC) and diminished expression of CD59, a membrane-bound protein that regulates MAC formation. Dr. Rohrer (left) is investigating therapeutic strategies to inhibit MAC through exclusive targeting of CD59 to membranes under attack. This strategy may have greater therapeutic potential than other approaches, since it can be administered either systemically or locally to bind specifically to affected membranes in diseases with restricted sites of inflammation such as AMD.

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