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

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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.

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