4.5 Article

Placental microRNA expression in pregnancies complicated by superimposed pre-eclampsia on chronic hypertension

期刊

MOLECULAR MEDICINE REPORTS
卷 14, 期 1, 页码 22-32

出版社

SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2016.5268

关键词

placenta; microRNA; pre-eclampsia; superimposed pre-eclampsia on chronic hypertension; pregnancy complication; Ion Torrent sequencing

资金

  1. Russian Federation President [16.120.11.5773 MC]
  2. Russian Scientific Foundation [14 50 00069]
  3. Russian Federation Government [074 U01]
  4. RF President scholarship [SP-1405.2015.4, SP-127.2015.4]

向作者/读者索取更多资源

Pre-eclampsia (PE) is a complication of pregnancy that affects 5-8% of women after 20 weeks of gestation. It is usually diagnosed based on the de novo onset of hypertension and proteinuria. Preexisting hypertension in women developing PE, also known as superimposed PE on chronic hypertension (SPE), leads to elevated risk of maternal and fetal mortality. PE is associated with an altered microRNA (miRNA) expression pattern in the placenta, suggesting that miRNA deregulation is involved in the pathogenesis of PE. Whether and how the miRNA expression pattern is changed in the SPE placenta remains unclear. The present study analyzed the placental miRNA expression profile in pregnancies complicated by SPE. miRNA expression profiles in SPE and normal placentas were investigated using an Ion Torrent sequencing system. Sequencing data were processed using a comprehensive analysis pipeline for deep miRNA sequencing (CAP-miRSeq). A total of 22 miRNAs were identified to be deregulated in placentas from patients with SPE. They included 16 miRNAs previously known to be associated with PE and 6 novel miRNAs. Among the 6 novel miRNAs, 4 were upregulated (miR-518a, miR-527, miR-518e and miR-4532) and 2 downregulated (miR-98 and miR-135b) in SPE placentas compared with controls. The present results suggest that SPE is associated with specific alterations in the placental miRNA expression pattern, which differ from alterations detected in PE placentas, and therefore, provide novel targets for further investigation of the molecular mechanisms underlying SPE pathogenesis.

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