Expression and role of miR‑338‑3p in peripheral blood and placenta of patients with pregnancy‑induced hypertension

Abstract

The present study aimed to investigate the role of miR-338-3p in pregnancy-induced hypertension (PIH), and its effects on human trophoblast cells in vitro. Quantitative real-time PCR was used to detect miR-338-3p expression. Human trophoblast HTR8/SVneo cells were transfected with miR-338-3p mimics. Effects of miR-338-3p on cell proliferation, invasion and metastasis, and anoikis resistance were detected by CCK-8 assay, Transwell chamber assay, flow cytometry and western blot analysis, respectively. Bioinformatics analysis was performed to predict the target of miR-338-3p, and the results were confirmed by dual luciferase reporter assay. The expression level of miR-338-3p was significantly upregulated in the peripheral blood and placenta of PIH patients. CCK-8 assay showed that miR-338-3p mimics inhibited the proliferation of HTR8/SVneo cells at indicated time points. Flow cytometry showed that miR-338-3p transfection significantly increased the Ki-67 expression in the HTR8/SVneo cells, indicating enhanced cell proliferation. Transwell chamber assay and western blot analysis showed that the invasion and metastatic abilities of the HTR8/SVneo cells were significantly decreased in the miR-338-3p transfection group, as well as expression levels of MMP-2 and MMP-9. Bioinformatics analysis and dual luciferase reporter assay indicated that AKT3 is a target gene of miR-338-3p. Our results suggest that miR-338-3p is significantly increased in the peripheral blood and placenta of PIH patients, which is correlated with the disease development. miR-338-3p inhibits proliferation, invasion and metastasis, and apoptosis resistance of human trophoblast cells by targeting AKT3.

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Placental homing peptide guides HIF1α‑silenced exosomes conjugates for targeted enhancement of invasion of trophoblast cells

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Analysis of Abnormal Expression of MiR-320b in Serum of Patients with Hypertension and its Clinical Value

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