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The major focus of our laboratory is to understand the cellular and molecular basis of retinal diseases that cause vision loss in humans, including both early onset diseases (such as Best vitelliform macular degeneration) and diseases associated with advancing age, such as age-related macular degeneration (AMD). We are especially interested in the role of the choroid in the development of AMD and other diseases. The choroid is an understudied layer of the eye containing a rich vascular supply that provides nutrients to the photosensitive rods and cones of the retina, as well as removing waste products. In addition to its role in nourishing the retina, the choroid plays important roles in retinal pathology in AMD, most notably when choroidal endothelial cells become activated to migrate, divide and invade the retina, which is characteristic of the severe neovascular or “wet” form of AMD. The responses of the choroidal microvasculature to stimuli occurring in diseased human eyes is a key area of focus in our group. We have found that fragments of the extracellular matrix protein elastin promote “disease-like” behaviors in these cells, including increased migration toward elastin fragments. These findings unite two observed events in AMD: elastin breakdown and choroidal endothelial cell activation. In addition, we are studying adhesion molecules produced by endothelial cells, such as immunoglobulin superfamily cell adhesion molecules, selectin family members and integrins, that are responsible for recruiting white blood cells from the lumen of small blood vessels into the tissue. We believe that these multidisciplinary studies--using human eyes, cell culture models, genetic analyses, and animal models--will provide important new insights into understanding how an eye progresses from a healthy state to early AMD and from early to advanced AMD.
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