Evidence map›Paper›PMID 35456471›Full record

ArticleGenes2022

MicroRNA-132-3p, Downregulated in Myeloid Angiogenic Cells from Hereditary Hemorrhagic Telangiectasia Patients, Is Enriched in the TGFβ and PI3K/AKT Signalling Pathways.

Anthony Cannavicci, Qiuwang Zhang, Marie E Faughnan, Michael J B Kutryk

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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  4. Review
  5. Article
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 1 institution in 1 country.

Anthony CannavicciInstitute of Medical Science, Cardiovascular Sciences Specialization Program, University of Toronto, Toronto, ON M5S 1A8, Canada.ORCID 0000-0001-7299-8891
Qiuwang ZhangKeenan Research Center for Biomedical Science, Division of Cardiology, St. Michael's Hospital, Unity Health Toronto, Toronto, ON M5B 1T8, Canada.
Marie E FaughnanInstitute of Medical Science, Cardiovascular Sciences Specialization Program, University of Toronto, Toronto, ON M5S 1A8, Canada.
Michael J B KutrykInstitute of Medical Science, Cardiovascular Sciences Specialization Program, University of Toronto, Toronto, ON M5S 1A8, Canada.
St. Michael's Hospital · CA

Funding

VCRC Administration UnitU54NS065705 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KIM, HELEN · 2009 to 2023
$20.8M
NINDS NIH HHS U54 NS065705
6 · The paper itself

Abstract

backgroundHereditary hemorrhagic telangiectasia (HHT) is a rare, autosomal dominant genetic disorder characterized by life-threatening vascular dysplasia. Myeloid angiogenic cells (MACs), alternatively called early endothelial progenitor cells or circulating angiogenic cells, do not directly incorporate into developing blood vessels, but augment angiogenesis in a paracrine manner. MAC dysfunction has been reported in HHT. MicroRNAs (miRNAs) regulate cellular function by modulating gene expression post-transcriptionally. To date, the role of miRNAs in HHT MAC dysfunction has not been documented.

objectiveThe goal of this study was to comparatively profile miRNAs in HHT patient and control MACs to identify dysregulated miRNAs that may be responsible for the observed MAC dysfunction in HHT. METHODOLOGY/

resultsTwenty-three dysregulated miRNAs (twenty-one upregulated and two downregulated) in HHT MACs were identified with a TaqMan miRNA microarray. Pathway enrichment analysis showed that the dysregulated miRNAs were significantly enriched in pathways involved in HHT pathogenesis, such as the transforming growth factor β (TGFβ), phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT), and Hippo signalling pathways. Furthermore, miR-132-3p was determined to be significantly reduced in HHT MACs compared with controls by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Bioinformatic analysis revealed that miR-132-3p is significantly enriched in the TGFβ and PI3K/AKT signalling pathways, targeting

conclusionMiRNA dysregulation, specifically reduced expression of miR-132-3p, in HHT MACs was identified. The dysregulated miRNAs are significantly enriched in the TGFβ, PI3K/AKT, and Hippo signalling pathways. These data suggest that alteration in miRNA expression may impair these pathways and contribute to MAC dysfunction in HHT.

Indexed as

MicroRNAsTelangiectasia, Hereditary HemorrhagicHumansp120 GTPase Activating ProteinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTransforming Growth Factor betaMicroRNAsMIRN132 microRNA, humanp120 GTPase Activating ProteinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRASA1 protein, humanTransforming Growth Factor betacirculating angiogenic cellsearly endothelial progenitor cellshereditary hemorrhagic telangiectasiamicroRNAsmyeloid angiogenic cellsPI3K/AKT signalling pathwaytransforming growth factor beta signalling pathway

Identifiers

PMID35456471
PMCPMC9027908
OpenAlexW4224262821

What OpenQuestion holds

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LicenceCC BY
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.