Choroidal neovascularization (CNV) represents the most common cause of severe vision loss in patients with age-related macular degeneration (AMD). It is also the most common cause of legal blindness in the United States in patients over the age of 60. Therefore, the study of the diagnosis, prevention and treatment of this condition would have a major impact on the public health. Based on evidence that vascular endothelial growth factor (VEGF) is upregulated in eyes with CNV associated with AMD, we have successfully produced CNV in an animal model by overexpressing VEGF in the retinal pigment epithelium through the use of subretinal delivery of an E-1deleted adenoviral vector encoding VEGF. For the past year, novel findings from this animal model have included: 1. The observation that bone marrow derived cells incorporate into the CNV and become part of the endothelium - blood vessel structure. By transplanting marked cells into the bone marrow of mice, these cells can be tracked and, following induction of CNV, were found in the lesion. This is the first example of bone marrow derived endothelial cells homing the site of CNV. 2. Further verification of the prominent choroidal changes that have been noted in this animal model were further elaborated. Intrachoroidal changes in these animals include a cellular response with macrophage infiltration, intrachoroidal new vessel formation and upregulated of choroidal ED-B fragment of fibronectin. 3. A biopsy specimen of a CNV from a patient was also examined and found to contain the simlar intrachoroidal changes as seen in the model.
