Evidence map›Paper›PMID 32035607›Full record

ArticleThe Journal of allergy and clinical immunology2020

An endothelial microRNA-1-regulated network controls eosinophil trafficking in asthma and chronic rhinosinusitis.

Asawari Korde, Farida Ahangari, Maria Haslip, Xuchen Zhang, Qing Liu, Lauren Cohn, Jose L Gomez, Geoffrey Chupp, Jordan S Pober, Anjelica Gonzalez and 1 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.6field-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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Roles of Exosomes in Chronic Rhinosinusitis: A Systematic Review.International journal of molecular sciences · 2022
    Pooled it
  2. Article
  3. Potential roles of microRNAs in chronic rhinosinusitis: from mechanistic insights to clinical studies.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026
    Article
  4. Article
  5. Review
  6. Causal role of MiRNAs in chronic rhinosinusitis: mendelian randomization and validation study.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Exosomes Derived fromMicrobiology spectrum · 2023
    Article
  18. Asthma Exacerbations: The Genes Behind the Scenes.Journal of investigational allergology & clinical immunology · 2023
    Review
  19. Review
  20. Review
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

11 authors at 1 institution in 2 countries.

Asawari KordeSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Conn.
Farida AhangariSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Conn.
Maria HaslipSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Conn; Yale School of Nursing, Orange, Conn.
Xuchen ZhangDepartment of Pathology, Yale School of Medicine, New Haven, Conn.
Qing LiuSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Conn.
Lauren CohnSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Conn.
Jose L GomezSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Conn.
Geoffrey ChuppSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Conn.
Jordan S PoberDepartment of Immunobiology, Yale School of Medicine, New Haven, Conn.
Anjelica GonzalezYale School of Engineering and Applied Science, New Haven, Conn.
Shervin S TakyarSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Conn. Electronic address: seyedtaghi.takyar@yale.edu.
Yale University · US

Funding

Functional role of hsa-miR-504 in airway inflammation and remodeling in asthmaK01HL125474 · NHLBI · YALE UNIVERSITY · PI GOMEZ-VILLALOBOS, JOSE LUIS · 2015 to 2019
$835k
MiR-1 is a Critical Regulator of VEGF-Induced AngiogenesisR00HL098695 · NHLBI · YALE UNIVERSITY · PI TAKYAR, SEYEDTAGHI · 2013 to 2015
$730k
A Cell-specific Endothelial MicroRNA Adenylation Pathway Regulates Th2 Inflammation in AsthmaR56AI125411 · NIAID · YALE UNIVERSITY · PI TAKYAR, SEYEDTAGHI · 2016 to 2016
$503k
NHLBI NIH HHS K01 HL125474NHLBI NIH HHS R00 HL098695NIAID NIH HHS R56 AI125411
6 · The paper itself

Abstract

backgroundAirway eosinophilia is a prominent feature of asthma and chronic rhinosinusitis (CRS), and the endothelium plays a key role in eosinophil trafficking. To date, microRNA-1 (miR-1) is the only microRNA known to be regulated in the lung endothelium in asthma models.

objectiveWe sought to determine the role of endothelial miR-1 in allergic airway inflammation.

methodsWe measured microRNA and mRNA expression using quantitative RT-PCR. We used ovalbumin and house dust mite models of asthma. Endothelium-specific overexpression of miR-1 was achieved through lentiviral vector delivery or induction of a transgene. Tissue eosinophilia was quantified by using Congo red and anti-eosinophil peroxidase staining. We measured eosinophil binding with a Sykes-Moore adhesion chamber. Target recruitment to RNA-induced silencing complex was assessed by using anti-Argonaute2 RNA immunoprecipitation. Surface P-selectin levels were measured by using flow cytometry.

resultsSerum miR-1 levels had inverse correlations with sputum eosinophilia, airway obstruction, and number of hospitalizations in asthmatic patients and sinonasal tissue eosinophilia in patients with CRS. IL-13 stimulation decreased miR-1 levels in human lung endothelium. Endothelium-specific overexpression of miR-1 reduced airway eosinophilia and asthma phenotypes in murine models and inhibited IL-13-induced eosinophil binding to endothelial cells. miR-1 recruited P-selectin, thymic stromal lymphopoietin, eotaxin-3, and thrombopoietin receptor to the RNA-induced silencing complex; downregulated these genes in the lung endothelium; and reduced surface P-selectin levels in IL-13-stimulated endothelial cells. In our asthma and CRS cohorts, miR-1 levels correlated inversely with its target genes.

conclusionEndothelial miR-1 regulates eosinophil trafficking in the setting of allergic airway inflammation. miR-1 has therapeutic potential in asthmatic patients and patients with CRS.

Indexed as

AnimalsAsthmaChemotaxis, LeukocyteEndothelial CellsEosinophilsHumansMiceMicroRNAsPulmonary EosinophiliaRhinitis, Allergic, PerennialSinusitisMicroRNAsMIRN1 microRNA, humanMirn1 microRNA, mouseasthmachronic rhinosinusitisEosinophil traffickingmicroRNAP-selectinvascular endothelium

Identifiers

PMID32035607
PMCPMC8440091
OpenAlexW3004768024

What OpenQuestion holds

Textmetadata
LicenceTDM
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.