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

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 in vitro. 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.

Automated summary

The study uncovered the crucial role of miR-302a in the pathogenesis of preeclampsia, showing that miR-302a can promote cell proliferation, migration, and invasion by targeting VEGFA, while inhibiting angiogenesis.