Evidence map›Paper›PMID 26227965›Full record

ArticleBMC pulmonary medicine2015

Protocadherin-1 is a glucocorticoid-responsive critical regulator of airway epithelial barrier function.

Yutaka Kozu, Yasuhiro Gon, Shuichiro Maruoka, Kuroda Kazumichi, Akiko Sekiyama, Hiroyuki Kishi, Yasuyuki Nomura, Minoru Ikeda, Shu Hashimoto

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05365841 (Role of Epithelial Barrier Integrity in Biologic Treatment Response of Severe Asthmatics With/Out Chronic Rhinosinusitis With Nasal Polyps), which is not on this map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.5field-weighted citation impact, top 12% 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.

NCT05365841 unknown statusnot on this mapstarted 2022, after this paper: background citation

Role of Epithelial Barrier Integrity in Biologic Treatment Response of Severe Asthmatics With/Out Chronic Rhinosinusitis With Nasal Polyps (CRSwNP). Can Shedding of Epithelial Barrier Proteins be Used as Biomarker in Severe Asthma With/Out CRSwNP Management?

TypeobservationalSponsorUniversity of CreteRan2022 to 2025Enrolled85ConditionsSevere Eosinophilic Asthma w/wo CRSwNPArmsMepolizumab 100 MG
3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Frontiers in immunology · 2026
    Article
  2. Review
  3. Article
  4. Tezepelumab: patient selection and place in therapy in severe asthma.The Journal of international medical research · 2024
    Review
  5. Effect of air pollution on asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Epithelial barriers in allergy and asthma.The Journal of allergy and clinical immunology · 2020
    Review
  10. Article
  11. Protocadherins at the Crossroad of Signaling Pathways.Frontiers in molecular neuroscience · 2020
    Review
  12. Article
  13. Article
  14. Hantavirus entry: Perspectives and recent advances.Advances in virus research · 2019
    Article
  15. Article
  16. Review
  17. Review
  18. Aberrant expression and functions of protocadherins in human malignant tumors.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  19. Article
  20. 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

9 authors at 1 institution in 1 country.

Yutaka KozuNihon University School of Medicine Division of Respiratory Disease, 30-1 Ohyaguchi-Kamicho, Itabashiku, Tokyo, 173-8610, Japan. blackflag@onyx.ocn.ne.jp.
Yasuhiro GonNihon University School of Medicine Division of Respiratory Disease, 30-1 Ohyaguchi-Kamicho, Itabashiku, Tokyo, 173-8610, Japan. gon.yasuhiro@nihon-u.ac.jp.
Shuichiro MaruokaNihon University School of Medicine Division of Respiratory Disease, 30-1 Ohyaguchi-Kamicho, Itabashiku, Tokyo, 173-8610, Japan. maruoka.shuichiro@nihon-u.ac.jp.
Kuroda KazumichiNihon University School of Medicine Division of Microbiology, 30-1 Ohyaguchi-Kamicho, Itabashiku, Tokyo, 173-8610, Japan. kuroda.kazumichi@nihon-u.ac.jp.
Akiko SekiyamaNihon University School of Medicine Division of Respiratory Disease, 30-1 Ohyaguchi-Kamicho, Itabashiku, Tokyo, 173-8610, Japan. akiko.wish@key.ocn.ne.jp.
Hiroyuki KishiNihon University School of Medicine Division of Otolaryngology, 30-1 Ohyaguchi-Kamicho, Itabashiku, Tokyo, 173-8610, Japan. kishi.hiroyuki@nihon-u.ac.jp.
Yasuyuki NomuraNihon University School of Medicine Division of Otolaryngology, 30-1 Ohyaguchi-Kamicho, Itabashiku, Tokyo, 173-8610, Japan. nomusan@siren.ocn.ne.jp.
Minoru IkedaNihon University School of Medicine Division of Otolaryngology, 30-1 Ohyaguchi-Kamicho, Itabashiku, Tokyo, 173-8610, Japan. ikeda.minoru@nihon-u.ac.jp.
Shu HashimotoNihon University School of Medicine Division of Respiratory Disease, 30-1 Ohyaguchi-Kamicho, Itabashiku, Tokyo, 173-8610, Japan. shuh@med.nihon-u.ac.jp.
Nihon University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImpaired epithelial barrier function renders the airway vulnerable to environmental triggers associated with the pathogenesis of bronchial asthma. We investigated the influence of protocadherin-1 (PCDH1), a susceptibility gene for bronchial hyperresponsiveness, on airway epithelial barrier function.

methodsWe applied transepithelial electric resistance and dextran permeability testing to evaluate the barrier function of cultured airway epithelial cells. We studied PCDH1 function by siRNA-mediated knockdown and analyzed nasal or bronchial tissues from 16 patients with chronic rhinosinusitis (CRS) and nine patients with bronchial asthma for PCDH1 expression.

resultsPCDH1 was upregulated with the development of epithelial barrier function in cultured airway epithelial cells. Immunocytochemical analysis revealed that PCDH localized to cell-cell contact sites and colocalized with E-cadherin at the apical site of airway epithelial cells. PCDH1 gene knockdown disrupted both tight and adhesion junctions. Immunohistochemical analysis revealed strong PCDH1 expression in nasal and bronchial epithelial cells; however, expression decreased in inflamed tissues sampled from patients with CRS or bronchial asthma. Dexamethasone (Dex) increased the barrier function of airway epithelial cells and increased PCDH1 expression. PCDH1 gene knockdown eradicated the effect of Dex on barrier function.

conclusionThese results suggest that PCDH1 is important for airway function as a physical barrier, and its dysfunction is involved in the pathogenesis of allergic airway inflammation. We also suggest that glucocorticoids promotes epithelial barrier integrity by inducing PCDH1.

Indexed as

Gene Expression RegulationAdultAgedAged, 80 and overApoptosisAsthmaBronchiCadherinsCells, CulturedEpithelial CellsFemaleGlucocorticoidsHumansImmunohistochemistryMaleMiddle AgedCadherinsGlucocorticoidsPCDH1 protein, humanProtocadherinsRNA

Identifiers

PMID26227965
PMCPMC4521469
OpenAlexW1862186887

What OpenQuestion holds

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Registered trials

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.