Abnormal placental angiogenesis, an important pathology during pregnancy, causes fetal growth retardation and preeclampsia in humans; small fetuses, hydrallantois, and abnormal placental development in cloned fetuses in farm animals. Normal vascular formation in the placenta is regulated by a dynamic gene transcription with some genes being parentally expressed. Using molecular technology and high-throughput data, we aim to elucidate the parental contribution in the regulation of placental angiogenesis. Our research model, the chorioallantois of the equine placenta, has a unique anatomical feature that facilitates the complete separation of the fetal and maternal compartment, allowing a reliable identification of parental contribution. In the murine and equine placenta, the paternally expressed RTL1 gene appears to play a crucial role in placental angiogenesis and is regulated by miR-127, a maternally expressed microRNA. However, this parental interaction has not yet been systematically confirmed. We hypothesize that the reciprocal parental interaction is essential for normal placental angiogenesis. Our research will provide fundamental information on the regulation of placental angiogenesis, can be extrapolated to other eutherian mammals, since our genes of interest are located on a preserved genomic region (DLK1-DIO3). Ultimately, this information will allow better diagnosis and treatment of abnormal angiogenesis and associated diseases during pregnancy.