Placenta­associated serum exosomal miR­155 derived from patients with preeclampsia inhibits eNOS expression in human umbilical vein endothelial cells.

Preeclampsia (PE) is considered to be initiated by abnormal placentation in early pregnancy and results in systemic endothelial cell dysfunction in the second or third trimester. MicroRNAs (miRs) expressed in the human placenta can be secreted into maternal circulation via exosomes, which are secreted extracellular vesicles that serve important roles in intercellular communication. The present study hypothesized that upregulation of placenta­associated serum exosomal miR­155 from patients with PE may suppress endothelial nitric oxide synthase (eNOS) expression in endothelial cells. The results demonstrated that placenta­associated serum exosomes from patients with PE decreased nitric oxide (NO) production and eNOS expression in primary human umbilical vein endothelial cells (HUVECs). Subsequently, an upregulation of placenta­associated serum exosomal miR­155 was detected in patients with PE compared with in gestational age­matched normal pregnant women. In addition, the results demonstrated that overexpression of exosomal miR­155 from BeWo cells was internalized into HUVECs, and was able to suppress eNOS expression by targeting its 3'­untranslated region. The results of the present study indicated that placenta­associated serum exosomes may inhibit eNOS expression in endothelial cell during PE development in humans, and this phenomenon may be partly due to increased miR­155 expression in placenta­associated serum exosomes.