Evaluation of Placentalmir-155-5p and Long Non-coding RNA sONE Expression in Patients with Severe Pre-eclampsia
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Faezeh Azizi1 , Soraya Saleh Gargari2 , Sedigheh Asadi Shahmirzadi3 , Fatemeh Dodange3 , Vahid Amiri4 , Reza Mirfakhraie1 , Mir Davood Omrani 5 |
1- Department of Medical Genetics, Faculty of Medicine, ShahidBeheshtiUniversity of Medical Sciences,Tehran, Iran. 2- Feto-Maternal Unit, ShohadayeTajrish Hospital, ShahidBeheshti, University of Medical Sciences, Tehran, Iran. 3- Feto-Maternal Unit, Mahdiyeh Hospital, ShahidBeheshti, University of Medical Sciences, Tehran, Iran. 4- School of Allied Medical Sciences,ShahidBeheshti, University of Medical Sciences, Tehran, Iran. 5- Department of Medical Genetics, Faculty of Medicine, ShahidBeheshtiUniversity of Medical Sciences,Tehran, Iran. , Davood_omrani@yahoo.co.uk |
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Abstract: (7179 Views) |
It has been well documented that preeclampsia (PE) has a common etiological background, but little is known about its linkage at the molecular level.Non- coding RNAs are critical posttranscriptional regulators ofgene expression. This study was performed to determine whether PEis associated with alterations in placental non-codingRNAs expression. MicroRNA(miR)-155-5p and long non-coding RNA (lnc)sONE expression, in placentas collected sequentially from 59 patients with PE and 40 normotensive pregnancies were measured using real-time PCR.The relationship between miR-155-5p and lncsONE expressions wasanalyzed statistically. miR-155-5p expression was increased(fold change=1.6, P=0.04), whilelncsONE expression was not significantly changed(fold change=1.1, P=0.68), in placentas from patients compared with control group.miR-155-5p was upregulated in placentas from patients with PEand may have influencedeNOS expression. These findings indicate that miRNA-155-5p may be involved in PE pathogenesis and could be a potential biomarker for this disease. |
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Keywords: Preeclampsia, miR-155-5p, long non-coding RNA sONE, real time PCR |
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Full-Text [PDF 712 kb]
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Type of Study: Original Article |
Subject:
Genetics & Disease Received: 2016/12/6 | Accepted: 2017/01/8 | Published: 2017/01/17
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