Scaring and uncontrolled neovascularization are components of several blinding disorders]. One of those diseases is age-related macular degeneration (AMD), a progressive disorder affecting the central region of the retina. It is the leading cause of blindness for Caucasians in the United States, with 6.5 % of the total population aged 40 years and older having symptoms of AMD to some degree. Dysfunction of the retinal support cells of the retinal pigmented epithelium (RPE) is generally considered to be central to the etiology of AMD. The RPE performs a number of unique functions essential for the sight and the maintenance of a healthy eye.
The first clinically recognized signs of AMD are the accumulation of macular extracellular deposits, named drusen, which stop the normal function of the eye. During these initial stages of the disease, classified as early AMD], there is minimal perceptible loss of vision. Prominent loss of vision is only associated with late or advanced AMD, which is characterized by deterioration and death of the RPE.
The transition from early to advanced AMD has features consistent with the onset of a wound response resulting from an underlying degenerative disease and chronic inflammation. We report findings directed at furthering our understanding of the molecular basis of RPE wound response, its likely impact on RPE function, and possible role in AMD. Using a cell culture model system coupled with a systems biology, we identify changes in expression in a number of genes encoding that play a role in wound response. Finally, we investigate the possible role for wound responses in AMD by comparing the changes in gene expression in this cell culture model to previously reported AMD-associated gene expression changes.