THE EXPRESSION AND MECHANISM OF ACTION OF MicroRNA-210 IN PREECLAMPSIA

Abstract

Background: MicroRNA-210 (miR-210) has been implicated in various diseases through its regulation of the Janus kinase–signal transducer and activator of transcription (JAK–STAT) signalling pathway. Despite this, its specific involvement in preeclampsia remains poorly understood. This study aims to investigate the role and pathogenesis of miR-210 and the JAK–STAT signalling pathway in patients with preeclampsia. Methods: In this study, 28 patients diagnosed with preeclampsia were allocated into a treatment group. Additionally, 22 pregnant women with preeclampsia were included as controls. Real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to assess the expression levels of miR-210, JAK2, and STAT3 mRNA. Human placental chorionic trophoblast cells were cultured in vitro and divided into three groups based on miR-210 transfection: the mimic, inhibition, and untransfected groups. Results: Compared with the control group, the expression level of miR-210 in the placenta of patients with preeclampsia was significantly higher (P < 0.05), and the levels of inflammatory factors such as interleukin (IL)-6 were positively correlated with the expression level of miR-210 in placental tissue. Analysis of CCK8 cell proliferation experiments showed that the cell proliferation rate in the mimic group was significantly higher compared to the inhibition and untransfected groups (P < 0.05). Flow cytometry analysis showed that the cell apoptosis rate in the mimic group was significantly lower than those of the inhibition and untransfected groups (P < 0.05). Compared with the untransfected group, the mRNA and protein expression levels of JAK2 and STAT3 in the mimic group were significantly higher, while those in the inhibition group were significantly lower (P < 0.05). Conclusion: In patients with preeclampsia, miR-210 may be involved in the proliferation and apoptosis of human placental trophoblast cells, which may be associated with the JAK2–STAT3 pathway and inflammatory responses. Further studies are warranted to clarify the precise molecular mechanisms underlying these associations.