Exosomal microRNA‑302a promotes trophoblast migration and proliferation, and represses angiogenesis by regulating the expression levels of VEGFA in preeclampsia

Abstract

The global morbidity rate of preeclampsia (PE) is 3‑7, and 10‑20% of maternal deaths are associated with PE. However, the mechanism of its pathogenesis remains unknown. The aim of the present study was to examine the relationship between microRNA‑302a (miR‑302a) and PE. Firstly, the relative expression levels of miR‑302a in placental tissues from patients with PE and normal controls were analyzed using reverse transcription‑quantitative PCR. miR‑302a expression was upregulated in PE tissues, particularly in severe PE. Subsequently, HTR‑8/SVneo cells were transfected with miR‑302a vectors to overexpress miR‑302a. The overexpression of miR‑302a markedly promoted cell proliferation, colony formation, migration and invasion <em>in vitro</em>. Subsequently, the present study examined the function of exosomes secreted by HTR‑8/SVneo cells transfected with miR‑302a vectors. Compared with the negative control vector group, miR‑302a expression was markedly increased in exosomes in the miR‑302a overexpression group. Additionally, exosomes with miR‑302a overexpression had repressed HUVEC invasion and ring formation. The luciferase reporter assay indicated that VEGFA was a direct target of miR‑302a, and miR‑302a expression was negatively correlated with VEGFA expression. In conclusion, the present results demonstrated that upregulation of miR‑302a may promote HTR‑8/SVneo cell proliferation, migration and invasion, and repress angiogenesis by targeting VEGFA, indicating that miR‑302a may be a potential target for the development of PE therapies.