Elevated microRNA-34a contributes to trophoblast cell apoptosis in preeclampsia by targeting BCL-2

J Hum Hypertens. 2017 Dec;31(12):815-820. doi: 10.1038/jhh.2017.65. Epub 2017 Oct 12.

Abstract

Preeclampsia (PE) is one of the most common pregnancy-specific pathologic complications, and is characterised by onset of hypertension and proteinuria. Placental trophoblast cell apoptosis is generally accepted as a major cause of PE. However, the details of the mechanism underlying the condition remain unclear. Here, we aimed to investigate a possible association between microRNA (miR)-34a and human trophoblast cell apoptosis during PE. We evaluated miR-34a expression in placentas from patients with PE compared with those from healthy pregnant individuals. Furthermore, we measured apoptosis rate after miR-34a mimic and/or inhibitor transfection in vitro, and identified B-cell CLL/lymphoma 2 (BCL-2) as a target of miR-34a. We found that miR-34a levels were significantly higher in placental tissues from patients with PE than in normal placentas. Upregulation of miR-34a induced trophoblast cell apoptosis in PE by inhibiting expression of BCL-2 protein. miR-34a inhibition reversed miR-34a-induced apoptosis in the HTR-8/SVneo human trophoblast cell line. Our findings indicate that miR-34a may be linked to the occurrence of PE via effects on BCL-2 in the human placenta, and may therefore provide a potential therapeutic target for PE.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Apoptosis
  • Case-Control Studies
  • Cell Line
  • Female
  • Humans
  • MicroRNAs / metabolism*
  • Pre-Eclampsia / etiology
  • Pre-Eclampsia / metabolism*
  • Pregnancy
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Trophoblasts / physiology*
  • Up-Regulation

Substances

  • MIRN34 microRNA, human
  • MicroRNAs
  • Proto-Oncogene Proteins c-bcl-2