Our goal is to determine how VEGF translation and transcription is affected by ER-stress and if this mechanism plays a role in experimental retinophathy. Recent publications have shown a correlation between ER-stress and increased levels of VEGF mRNA and protein. Protein synthesis attenuation occurs during ER-stress and has prompted us to examine the role of a proposed internal ribosome entry site (IRES), located in the 5' UTR, in the translation initiation of VEGF synthesis. The role of ER-stress on angiogenesis will be further explored using an in vitro diabetic retinopathy model. The Streptozotocin (STZ) and retinopathy of prematurity (ROP) diabetic rat models are the identified models in which these studies will take place. By confirming or disproving the role of ER-stress on angiogenesis we will develop a greater understanding of vascular associated complications seen in diabetes.