256-POS

Abstract

Objectives Vitamin D insufficiency is associated with a 5-fold increased risk for development of preeclampsia. We hypothesize that vitamin D plays an important role in the health of endothelial progenitor cells that participate in maternal and placental vasculogenesis and vascular endothelial repair. We asked if vitamin D antagonizes the negative effects of preeclampsia, or a preeclampsia-like environment, on fetal endothelial progenitor cell function. Methods Umbilical cord blood was obtained from preeclamptic and uncomplicated pregnancies. The mononuclear cells were isolated and seeded onto culture plates for outgrowth of endothelial colony forming progenitor cells (ECFCs). Placental explants from uncomplicated term pregnancies were incubated for 48 h under 2%, 8% or 21% O2. Explant conditioned media (CM) was collected and pooled according to oxygen level. Migration, proliferation, and tubule formation of ECFCs was determined in the presence/absence of CM or maternal serum, and 1,25(OH)2 vitamin D3. We inhibited the VEGF signaling pathway with Su5416 and blocked the VDR with VDR antagonist pyridoxal-5-phosphate or antiVDR siRNA. Results The number of cord blood-derived ECFC colonies was decreased in PE compared with controls (P = 0.04). Preeclampsia ECFCs showed reduced proliferation (P Conclusions Physiological concentrations of vitamin D3 promote the migration and capillary-like tubule formation of ECFCs in culture, minimizing negative effects of preeclampsia or preeclampsia-related factors. Such positive effects of vitamin D on progenitor cell function might improve placental and endothelial function and pregnancy outcome. Disclosures L. Brodowski: None. J. Burlakov: None. C.A. Hubel: None. F. von Versen-Hoynck: None.