Angiogenesis Research Laboratory
The Powers' lab uses a mouse model of retinopathy of prematurity (ROP) to investigate the balance between angiogenic cytokines and pro-apoptotic factors in retinal neovascularization. In vitro studies using retinal endothelial cells are used to study intracellular pathways of apoptosis. Our ongoing studies use ocular neovascularization as a valuable model system but our results will also shed light on the basic biological processes of pathological angiogenesis. Our studies have broad applicability to other disease such as diabetic retinopathy, asthma, heart disease, hemangiomas, as well as childhood cancer and metastasis. The laboratory is located on the 2nd floor of the Biomedical Research Building in the Casey Eye Institute Laboratories.
Retinopathy of prematurity (ROP) continues to affect thousands of infants each year. The incidence of ROP is closely related to the degree of prematurity at birth. Ablative treatments with laser therapy for progressive ROP can reduce the risk for retinal detachment, but 45% of these eyes progress to blindness. The Powers' lab uses the mouse model of oxygen induced retinopathy (OIR) to investigate the role of cytokines and apoptosis in retinal neovascularization (NV). This model was developed by Smith and colleagues in the early 1990s and has become the gold standard for research on retinal angiogenesis. Studies in mice have created a fundamental understanding of blood vessel guidance, the role of vascular endothelial cell growth factor (VEGF) isoforms in both normal and pathologic retinal NV, the critical interactions of retinal endothelial cells and mural cells, and the role of apoptosis in the balance between angiogenic and anti-angiogenic factors. Dr. Powers' research is currently focused on the role of apoptosis in vascular regression of pathologic retinal neovascularization. The ultimate goal is to modulate apoptosis in order to promote regression of pathologic vessels thereby preventing retinal detachment and vision loss in premature infants.