HDAC4 Knockdown Induces Preeclampsia Cell Autophagy and Apoptosis by miR-29b

Preeclampsia (PE) is one of the main causes of maternal death and perinatal morbidity and mortality. Considering that histone deacetylase 4 (HDAC4) activity could relate to trophoblast cell motility and be antagonized by miR-29b, the aim of the present study was to investigate the ability of HDAC4 to regulate placental trophoblast cells by miR-29b. We assessed the cytological changes of PE patients, and the expression and cellular localization of HDAC4 and LC3 by histological analysis, immunohistochemistry, western blot assay, and immunofluorescence staining assay. We observed the effect of hypoxia on HDAC4, the correction of HDAC4/miR-29b, and the effects of HDAC4/miR-29b on HTR8 cells by dual-luciferase, quantitative real-time PCR, western blot assay, and flow cytometry assay. Here, we first found that HDAC4 was lowly expressed in PE tissues, while LC3 was highly expressed. In addition, the expression of HDAC4 was inhibited by hypoxia in HTR8 cells. Furthermore, our data showed that HDAC4 activity could be antagonized by miR-29b. We highlighted that miR-29b specifically targeted HDAC4 in trophoblast cells and both molecules were involved in a functional loop. Altogether, our findings demonstrated that silencing of HDAC4 could trigger cell autophagy and apoptosis directly by miR-29b in placental trophoblast cells of PE.