Neovascularization of the retina and choroids is the pathological hallmark of many retinopathies, but its molecular mechanisms remain unclear. Vascular endothelial growth factor (VEGF), which is induced by hypoxia or cytokines, plays a critical role in the abnormal growth of blood vessels. In the study, we reports that visible light exposure induces VEGF gene expression in retinoblastoma Y 79 cells. Fluorescent light exposure (700 lux, wavelength 400~740 nm) caused a significant increase in VEGF transcripts and protein levels. Such an induction seemed to be specific to a cells including photoreceptor cells because light-induced VEGF expression was not observed in either nontransformed cells such as retinal pigment epithelium (RPE) cells and BEAC or transformed such as CV-1 and HepG2 cells. Pertussis toxin and guanosine 5'- [beta-thio] diphosphate (GDPs), a specific inhibitors for rhodopsin- associated G protein, blunted this induction. Progressive deletion and site-specific mutation analyses indicate that light stimulation increase VEGF promoter activity through G+C-rich sequence which is proved as Sp1-binding sites by supershift assays. Electrophoretic mobility shift assays (EMSAs) show that Sp1 binding is increased by light stimulation. Synthetic retinoic acid receptor-(RAR)antagonist completely abrogated light-mediated increase in VEGF expression. Transfection of Y79 cells with dominant negative mutant of RAR significantly attenuated the light-mediated induction of VEGF promoter activity. In conclusion, our data indicate that light exposure increases VEGF expression through the mechanisms involving activation of Sp1 and RAR signaling in Y79 cells. This study provides the new insight into the role of visible light in the transcription and induction of VEGF gene expression.