Expression and clinical significance of miR-377-3p and cyclin G2 in preeclampsia patients.

BACKGROUND AND OBJECTIVES: Numerous studies have demonstrated that differentially expressed microRNA (miRNA) play a crucial role in the pathophysiology of preeclampsia (PE). These miRNA are central to ongoing investigations into the pathogenesis of PE. This study aims to investigate the relationship between changes in miR-377-3p and cell cyclin G2 (CCNG2) expression and the clinical features of PE, as well as to further analyze the effect of miR-377-3p on CCNG2. METHODS: A total of 120 pregnant subjects were recruited, consisting of 70 PE cases and 50 healthy pregnancies. The expression levels of miR-377-3p and CCNG2 mRNA were detected through RT-qPCR, while the protein expression of CCNG2 was examined via Western blot. The Pearson test was employed to analyze the relationship between miR-377-3p and CCNG2 mRNA expression and clinical parameters related to PE. The effect of miR-377-3p on CCNG2 was verified using a dual-luciferase reporter assay. RESULTS: Compared with normal controls, miR-377-3p was significantly down-regulated in PE plasma and placental tissues, while CCNG2 was up-regulated (P < 0.05). The abnormal expression of both miR-377-3p and CCNG2 was associated with the severity of PE. The expression of miR-377-3p and CCNG2 mRNA in the plasma and placenta of PE patients was significantly correlated with systolic blood pressure (SBP), diastolic blood pressure (DBP), and neonatal birth weight (P < 0.05). Moreover, miR-377-3p and CCNG2 were consistently expressed in plasma and placental tissues (r = 0.521, P < 0.01; r = 0.247, P = 0.039), and the expression of the two was negatively correlated (plasma: r = - 0.475, P < 0.05; placental: r = - 0.497, P < 0.05). The dual-luciferase reporter assay confirmed that miR-377-3p negatively regulated CCNG2 expression in HTR-8/SVneo cells. CONCLUSION: The low expression of miR-377-3p, alongside the high expression of CCNG2 in the peripheral plasma and placental tissues of PE patients, may be linked to the onset of the condition. These findings suggest that miR-377-3p may contribute to the development of PE by regulating the expression of CCNG2.