Upregulation of MiR-29b contributes to mesenchymal stem cell dysfunction in patients with severe pre-eclampsia

The aim of this study was to investigate the role of miR-29b in the regulation of decidua-derived mesenchymal stem cells (dMSCs) to influence the pathogenesis of pre-eclampsia (PE). dMSCs were isolated from decidua tissue and characterized. The expression of miRNAs was evaluated by quantitative PCR. Overexpression and inhibition of miR-29b were achieved in dMSCs, and the effect of miR-29b overexpression on the migration and angiogenic potential of human umbilical vein endothelial cells (HUVEC) was assessed. Furthermore, we performed bioinformatic analyses, luciferase reporter gene assays, and gene expression analyses to identify the potential targets of miR-29b and to verify the effect of target genes on dMSC function. Upregulation of miR-29b was confirmed in severe PE patients. Overexpression of miR-29b attenuated cell proliferation of dMSCs. Overexpression of miR-29b in dMSCs decreased the migratory and tubule formation ability of HUVECs. Histone deacetylase 4 (HDAC4) was identified as a target gene of miR-29b. Decreased migration and tubule formation in HUVECs was observed upon incubation with conditioned medium from dMSCs treated with the HDAC inhibitor trichostatin A. Our results demonstrated that upregulation of miR-29b in dMSCs has an important paracrine effect and might be involved in the development of PE.