Dr. Ammar has a broad-based background in vision research combining biochemistry, cell biology, and cell physiology. He has extensive experience with epithelial and endothelial cells, specialized cells that line the interior of the eye. These cells perform critical functions that support the proper function of the retina, such as ion and metabolite transport, fluid production, tissue remodeling and fluid outflow. Dr. Ammar collaborates with other Department of Ophthalmology faculty in several research areas. A current collaboration with Drs. Kahook
involves using laser-assisted multiphoton microscopy to image regions of the eye involved in Glaucoma
. This work brings together a group of investigators with complementary skills and expertise, and our recent publication was one of the first to see fluid outflow structures in the intact human and mouse eyes. A second collaboration with Dr. Petrash
involves understanding the mechanisms of diabetic eye diseases, cataract formation, and retinal degeneration. Dr. Ammar also has fifteen years of experience in live-cell imaging and as well as knowledge of specialized microscopy, and currently collaborates with Dr. Petrash’s lab to image fluorescently-tagged proteins in live cells. Various other research projects include in vitro toxicity assays using various ocular cells to test the effects of various drugs, chemicals, and surgical devices.
As part of his departmental duties, Dr. Ammar heads the Department of Ophthalmology Research Histology Core. The eye is an organ containing several different tissue types that requires specialized histological expertise. Dr. Ammar oversees the work of Pat Lenhart, our histologist, to provide assistance to researchers who require histological stains in paraffin sections and immunofluorescence stains in cryo-sections.
Glaucoma is the second leading cause of blindness in the United States, affecting approximately more than 2 million adults. The risk of glaucoma increases with age, with an incident rate of ~1% at age 40 to increasing to >5% at age 70. Although glaucoma is a neurodegenerative disease of the retina, the primary cause of glaucoma is believed to be dysfunction of aqueous humor (AH) outflow resulting in increased intraocular pressure (IOP).
AH fluid is produced in the ciliary body, and most of the fluid exits the eye through the angle of the eye (a pocket formed at the junction of the iris and cornea). The outflow structures consist of the trabecular meshwork, Schlemm’s canal, and collector channels. Dysfunction of these structures is believed to be directly linked to a reduction in fluid outflow, resulting in increased IOP. However, these structures are hidden within the opaque scleral tissue and cannot be directly imaged.
Therefore, current diagnosis of glaucoma depends on either detecting loss of visual function or detecting specific structural changes to the retina. However, small structural changes to the retina and visual field may not diagnostic glaucoma, while large changes suggest that the disease has already progressed. Since nerve damage is irreversible, early diagnosis and detection is the most effective way to limit damage to the retina and prevent disease progression. Developing new technologies to accurately track structural and functional changes within the outflow structures of the eye would allow earlier diagnosis as well as enable us to monitor the effectiveness of medical intervention. This could potentially prevent premature blindness in millions of patients.
Our publications demonstrate the ability to utilize multi-photon microscopy (MPM) to obtain high-resolution (~1 µm) three-dimensional images of the intact mouse eye. MPM has been used to perform label-free measurements to quantify the structure of the extracellular collagen matrix, characterize the size and shape of Schlemm’s canal and collector channels, and measure the state of oxidative stress of epithelial cells located in the trabecular meshwork. Using a custom-built MPM imaging platform, we have successfully imaged the mouse eye in situ.