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

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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Acknowledgements

This study was supported by the Science and Technology Grant from Education Department of Heilongjiang Province, China (12521347). MG and PL conceived and designed the experiments. MG, XX and XY performed the experiments. MG and XY analysed data and wrote the manuscript. PL reviewed and edited the manuscript.

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Correspondence to P Li.

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Guo, M., Zhao, X., Yuan, X. et al. Elevated microRNA-34a contributes to trophoblast cell apoptosis in preeclampsia by targeting BCL-2. J Hum Hypertens 31, 815–820 (2017). https://doi.org/10.1038/jhh.2017.65

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