RESUMEN
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.