Placental-derived Exosomal Mir-125B Disrupts Maternal Endothelial Function in Preeclampsia

Preeclampsia (PE) is an elusive life-threatening complication of pregnancy, and maternal endothelial dysfunction induced by components from the impaired placenta is a key hallmark of PE. Placenta-derived exosomes in maternal circulation has been reported with increased risk of PE, however, whether exosomes impaired endothelial cell function remains to be determined. We hypothesized that placental exosomes from preeclamptic patients disrupt endothelial function. We observed that placenta derived serum exosomes from preeclamtpic patients (PE-exo) significantly reduced VE-cadherin expression in primary cultured human umbilical vein endothelial cells (HUVECs), thus resulting in increased endothelial permeability. Realtime qPCR results indicated more miR‑125b in PE-exo. Moreover, we identified that VE-cadherin was a direct target of exosomal miR-125b in HUVECs. miR-125b could partly mediates the adverse effect of PE-exo on endothelial functions. Our findings suggest that miR-125b derived from placental exosomes is involved in the progression of PE and could be a promising therapeutic target for PE. This work was funded by grants from the Natural Science Foundation of Shandong Province (ZR2022MH195, ZR2019BH037), Graduate Student Research Grant from Weifang Medical University This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.