327. Shedding of the placental glycocalyx in response to ischemia and hypoxia

Introduction Placental ischemia appears to be a central causative factor in the maternal symptoms of preeclampsia. The maternal/fetal interface in the placenta is covered in a meshwork resembling the endothelial glycocalyx; consisting of proteoglycans like Syndecan-1 (SDC-1). This glycocalyx is essential for preventing immune cell adherence, and shed glycocalyx fragments are pro-inflammatory. Objective/Hypothesis We hypothesize that hypoxia/ischemia will cause degradation and shedding of the placental glycocalyx. Methods Placental ischemia was studied using the rodent RUPP model, which induces placental ischemia from GD14–19. Acute hypoxia utilized culture BeWo trophoblasts exposed at 8% or 1% oxygen for 24 h to simulate the normal or ischemic placenta respectively. SDC-1 was measured via western blot in placenta and by commercial ELISA in cell culture. Results RUPP rats showed a significant decrease in placental syndecan-1 compared to sham controls (100 ± 33% vs 67 ± 17%, p  Discussion Placental ischemia and acute hypoxia both contribute to trophoblast shedding of the placental glycocalyx in a manner dependent on heparanase, MMP activity, and oxidative stress.