Evidence map›Paper›PMID 28148930›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2017

MiR-126a-5p is involved in the hypoxia-induced endothelial-to-mesenchymal transition of neonatal pulmonary hypertension.

Yan-Ping Xu, Qi He, Zheng Shen, Xiao-Li Shu, Chen-Hong Wang, Jia-Jun Zhu, Li-Ping Shi, Li-Zhong Du

Abstract read
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In one paragraph

Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.1field-weighted citation impact, top 6% 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, 38 citations in OpenAlex.

  1. Review
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  10. Analysis of miRNAs Involved in Mouse Heart Injury Upon Coxsackievirus A2 Infection.Frontiers in cellular and infection microbiology · 2022
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  17. Circular RNAs in hypertension: challenges and clinical promise.Hypertension research : official journal of the Japanese Society of Hypertension · 2019
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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 2 institutions in 1 country.

Yan-Ping XuNICU, The Children's Hospital, Zhejiang University School of Medicine, Zhejiang Key Laboratory for Diagnosis and Therapy of Neonatal Diseases, Hangzhou, China.
Qi HeNICU, The Children's Hospital, Zhejiang University School of Medicine, Zhejiang Key Laboratory for Diagnosis and Therapy of Neonatal Diseases, Hangzhou, China.
Zheng ShenCenter Lab, Children's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xiao-Li ShuCenter Lab, Children's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Chen-Hong WangNICU, The Children's Hospital, Zhejiang University School of Medicine, Zhejiang Key Laboratory for Diagnosis and Therapy of Neonatal Diseases, Hangzhou, China.
Jia-Jun ZhuDepartment of Neonatology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Li-Ping ShiNICU, The Children's Hospital, Zhejiang University School of Medicine, Zhejiang Key Laboratory for Diagnosis and Therapy of Neonatal Diseases, Hangzhou, China.
Li-Zhong DuNICU, The Children's Hospital, Zhejiang University School of Medicine, Zhejiang Key Laboratory for Diagnosis and Therapy of Neonatal Diseases, Hangzhou, China.
Children's Hospital of Zhejiang University · CNWomen's Hospital, School of Medicine, Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent pulmonary hypertension of the newborn (PPHN) is a clinical syndrome characterized by increased medial and adventitial thickness of the lung vasculature. The underlying mechanisms that regulate the cell phenotype alteration during PPHN remodeling are largely unknown. We randomly selected newborn rats that were exposed to hypoxia (10-12%) or room air for 2 weeks and used a microarray to identify the lung tissue microRNAs (miRNAs) involved in PPHN progression. The role of a key miRNA that affects the endothelial-to-mesenchymal transition (EndMT) in primary cultured rat pulmonary microvascular endothelial cells (RPMECs) was investigated. The expression of miR-126a-5p was elevated in the PPHN model according to microarray analysis. The relative expression of miR-126a-5p in RPMECs increased when they were exposed to hypoxia (P<0.05), consistent with the microarray results. Pecam1 expression decreased, whereas alpha-smooth muscle actin (α-SMA) increased in the hypoxic RPMECs. Knockdown of miR-126a-5p in RPMECs followed by treatment with hypoxia for 48 h resulted in a significant increase in the expression of Pecam1 and a reduction in α-SMA expression, with a simultaneous increase in PI3K (p85β) and phosphorylation of AKT at serine 473 compared with the negative control. Finally, the circulating miR-126a-5p concentration was upregulated in the PPHN model compared with healthy neonates. We concluded that hypoxia changed the cell homeostasis and that miR-126a-5p was upregulated in PPHN, which is partly responsible for hypoxia-induced EndMT. The mechanism underlying the upregulation of miR-126a-5p by hypoxia probably acts through the p85-β/p-AKT pathway.

Indexed as

Cell TransdifferentiationAnimalsAnimals, NewbornCells, CulturedEndothelial CellsGene Expression ProfilingHumansInfant, NewbornLungMicroRNAsOligonucleotide Array Sequence AnalysisPersistent Fetal Circulation SyndromePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRandom AllocationRats, Sprague-DawleyMicroRNAsMIRN126 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID28148930
OpenAlexW2583166589

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.