Preeclampsia (PE) is a leading cause of maternal and perinatal morbidity and mortality, affecting 3 to 8% of all pregnancies. Current research suggests that the impaired trophoblastic invasion and remodeling of maternal spiral arteries contributes significantly to the development of PE. However, the pathobiology of PE remains poorly understood, and there is a lack of screening methods and treatment options largely due to ineffective experimental models of PE. Utilizing the capability of bioprinting, we hypothesize that the architecture of the maternal spiral arteries and stiffness of the maternal decidua are effective predictors for preeclampsia because they (1) alter the chemoattractant concentration that drives trophoblastic invasion and (2) impair the migratory and invasive response of trophoblasts. To test our hypothesis, we aim to bioprint a bioengineered placenta model to assess preeclamptic and healthy trophoblast migration. Together with our collaborators in Children’s National Medical Center, our work will be the first step to develop and validate the much needed predictors to screen for preeclampsia before the second trimester. This works thus has the potential to save the lives of mothers and children, and transform the current clinical practices for screening and predicting preeclampsia. We believe that our bioengineered placenta model will be a powerful tool for researchers to test and to develop novel treatments for preeclampsia that could revolutionize the field.