Mutations in the human Endoglin gene, encoding a dimeric TGF-beta co-receptor, lead to type 1 hereditary hemorrhagic telangiectasia. Studies in mice have revealed important roles of Endoglin in endothelial cell proliferation, differentiation and integrity. Endoglin(-/-) mouse embryos die at mid-gestation due to cardiac defects and vessel rupture. Its role during early vasculogenesis is unclear, as the initial phase of vascular endothelial cell formation appears unaffected in Endoglin(-/-) embryos. In order to understand possible roles of Endoglin in early vascular development, we used the chick model and analyzed the temporal and spatial expression pattern of Endoglin during vasculogenesis in pre-circulation stage chick embryos. Weak Endoglin expression was detected at HH4 in the node and in the extraembryonic mesoderm. The node-specific expression is transitory and disappears after HH5. Strong up-regulation of Endoglin expression is seen at HH8 in all endothelial progenitors undergoing morphological changes to become endothelial cells. Most extraembryonic splanchnopleural vascular endothelial cells down-regulate Endoglin after their morphological differentiation, whereas lateral plate and cardiac endothelial cells remain positive until HH12, followed by a clear drop after circulation starts at HH13. Progenitors for the pronephric duct are positive from HH10 to HH12, but down-regulate Endoglin after epithelialization of duct cells. Overall, these data reveal a dynamic expression pattern of Endoglin in pre-circulation chick development and indicate that Endoglin may play an important role in the transition from endothelial progenitors to functional endothelial cells during early vascular development.