Evidence map›Paper›PMID 28393453›Full record

ArticleJournal of cellular and molecular medicine2017

Novel mechanism of miRNA-365-regulated trophoblast apoptosis in recurrent miscarriage.

Wei Zhao, Wei-Wei Shen, Xiao-Mei Cao, Wen-Yan Ding, Lin-Ping Yan, Ling-Juan Gao, Xiu-Ling Li, Tian-Ying Zhong

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 55 citations in OpenAlex.

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  18. Estrogen Receptors and Estrogen-Induced Uterine Vasodilation in Pregnancy.International journal of molecular sciences · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Wei ZhaoThe Fourth School of Clinical Medicine of Nanjing Medical University, Nanjing, China.
Wei-Wei ShenState Key Laboratory of Reproductive Medicine, Department of Clinical Laboratory, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Tianfei Alley, Nanjing, China.
Xiao-Mei CaoDunman High School, Singapore City, Singapore.
Wen-Yan DingState Key Laboratory of Reproductive Medicine, Department of Clinical Laboratory, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Tianfei Alley, Nanjing, China.
Lin-Ping YanThe Fourth School of Clinical Medicine of Nanjing Medical University, Nanjing, China.
Ling-Juan GaoState Key Laboratory of Reproductive Medicine, Department of Clinical Laboratory, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Tianfei Alley, Nanjing, China.ORCID 0000-0002-9500-3639
Xiu-Ling LiState Key Laboratory of Reproductive Medicine, Department of Clinical Laboratory, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Tianfei Alley, Nanjing, China.
Tian-Ying ZhongState Key Laboratory of Reproductive Medicine, Department of Clinical Laboratory, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Tianfei Alley, Nanjing, China.
Nanjing Medical University · CNSecond Affiliated Hospital of Nanjing Medical University · CNShimano (Singapore) · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical pregnancies increasingly end in recurrent miscarriage (RM) during the first trimester, with genetic factors shouldering the main responsibility. MicroRNAs (miRNAs) regulate gene expression in a wide array of important biological processes. We examined the potential role of dysregulated miRNAs in RM pathogenesis and trophoblast development as an approach to elucidate the molecular mechanism behind RM. miRNA profiles from clinical specimens of RM and induced abortion (IA) were compared, and several miRNAs were found to be aberrantly expressed in RM samples. Among the miRNAs, miR-365 was significantly differentially expressed in RM decidual tissues. Furthermore, our results demonstrate that miR-365 functions as an upstream regulator of MDM2/p53 expression, cell cycle progression and apoptosis in trophoblasts. Bioinformatic prediction and experimental validation assays identified SGK1 as a direct target of miR-365; consistently, its protein levels were low in decidual tissues. Additionally, functional studies revealed that SGK1 silencing elicits cell cycle arrest and apoptosis in trophoblasts and that SGK1 overexpression attenuates the effects of miR-365 on apoptosis and MDM2/p53 expression. Collectively, our data provide evidence that the up-regulation of miR-365 may contribute to RM by decreasing SGK1 expression, which suggests its potential utility as a prognostic biomarker and therapeutic target for RM.

Indexed as

Gene Expression Regulation3' Untranslated RegionsAbortion, HabitualAbortion, InducedAdultApoptosisCell Cycle CheckpointsCell LineFemaleGene Expression ProfilingHumansImmediate-Early ProteinsMicroRNAsMicroscopy, Electron, TransmissionPregnancyProtein Serine-Threonine Kinases3' Untranslated RegionsImmediate-Early ProteinsMicroRNAsMIRN-3662 microRNA, humanProtein Serine-Threonine KinasesProto-Oncogene Proteins c-mdm2Serum-Glucocorticoid Regulated KinasesapoptosisGlucocorticoid inducible kinase 1mechanismmiRNA-365Recurrent miscarriage

Identifiers

PMID28393453
PMCPMC5618703
OpenAlexW2607232908

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.