Evidence map›Paper›PMID 25077964›Full record

ArticleThe Journal of biological chemistry2014

MicroRNA regulation of mitogenic signaling networks in the human placenta.

Farkhondeh Farrokhnia, John D Aplin, Melissa Westwood, Karen Forbes

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  4. The role of microRNAs in pregnancies complicated by maternal diabetes.Clinical science (London, England : 1979) · 2024
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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

4 authors at 3 institutions in 1 country.

Farkhondeh FarrokhniaMaternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, Manchester M13 9WL, United Kingdom and; St. Mary's Hospital, Central Manchester University Hospitals National Health Service Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom.
John D AplinMaternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, Manchester M13 9WL, United Kingdom and; St. Mary's Hospital, Central Manchester University Hospitals National Health Service Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom.
Melissa WestwoodMaternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, Manchester M13 9WL, United Kingdom and; St. Mary's Hospital, Central Manchester University Hospitals National Health Service Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom.
Karen ForbesMaternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, Manchester M13 9WL, United Kingdom and; St. Mary's Hospital, Central Manchester University Hospitals National Health Service Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 9WL, United Kingdom. Electronic address: karen.forbes@manchester.ac.uk.
Manchester Academic Health Science Centre · GBNational Health Service · GBUniversity of Manchester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Placental cell growth depends on an adaptable combination of an endogenous developmental program and the exogenous influence of maternal growth factors, both of which may be influenced by microRNA (miR)-dependent effects on gene expression. We have previously shown that global miR suppression in placenta accelerates proliferation and enhances levels of growth factor signaling mediators in cytotrophoblast. This study aimed to identify miRs involved in regulating placental growth. An initial array revealed 58 miR species whose expression differs between first trimester, when cytotrophoblast proliferation is rapid, and term, by which time proliferation has slowed. In silico analysis defined potential growth-regulatory miRs; among these, hsa-miR-145, hsa-miR-377, and hsa-let-7a were predicted to target known placental growth genes and were higher at term than in the first trimester, so they were selected for further analysis. Overexpression of miR-377 and let-7a, but not miR-145, in first trimester placental explants significantly reduced basal cytotrophoblast proliferation and expression of ERK and MYC. PCR arrays, in silico analysis, Western blotting, and 3'-UTR luciferase reporter assays revealed targets of miR-145 within the insulin-like growth factor axis. Analysis of proliferation in placental explants overexpressing miR-145 demonstrated its role as a mediator of insulin-like growth factor-induced trophoblast proliferation. These findings identify miR-377 and let-7a in regulation of endogenous cell growth and miR-145 in the placental response to maternal stimulation and will aid the development of therapeutic strategies for problem pregnancies.

Indexed as

Cell LineCell ProliferationFemaleGene Regulatory NetworksHumansMicroRNAsMitosisPlacentaPregnancyPregnancy Trimester, FirstRNA InterferenceSignal TransductionSomatomedinsTranscriptomeTrophoblastsMicroRNAsMIRN145 microRNA, humanMIRN377 microRNA, humanmirnlet7 microRNA, humanSomatomedinsDevelopmental FactorGene RegulationInsulin-like Growth Factor (IGF)MicroRNA (miRNA)PlacentaProliferationReproductionTrophoblast

Identifiers

PMID25077964
PMCPMC4215224
OpenAlexW2008586030

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.