Evidence map›Paper›PMID 31664154›Full record

ArticleScientific reports2019

Osteopontin Expression in Small Airway Epithelium in Copd is Dependent on Differentiation and Confined to Subsets of Cells.

Mohamad N Ali, Michiko Mori, Tinne C J Mertens, Premkumar Siddhuraj, Jonas S Erjefält, Patrik Önnerfjord, Pieter S Hiemstra, Arne Egesten

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
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  10. Article
  11. Article
  12. Osteopontin Deficiency Ameliorates Prostatic Fibrosis and Inflammation.International journal of molecular sciences · 2021
    Article
  13. Article
  14. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 3 countries.

Mohamad N AliRespiratory Medicine & Allergology, Department of Clinical Sciences Lund, Lund University and Skåne University Hospital, Lund, Sweden. Mohamad.Ali@med.lu.se.
Michiko MoriUnit of Airway Inflammation, Department of Experimental Medical Sciences, Lund University and Skåne University Hospital, Lund, Sweden.
Tinne C J MertensDepartment of Pulmonology, Leiden University Medical Center, Leiden, The Netherlands.
Premkumar SiddhurajUnit of Airway Inflammation, Department of Experimental Medical Sciences, Lund University and Skåne University Hospital, Lund, Sweden.
Jonas S ErjefältUnit of Airway Inflammation, Department of Experimental Medical Sciences, Lund University and Skåne University Hospital, Lund, Sweden.
Patrik ÖnnerfjordRheumatology & Molecular Skeletal Biology, Department of Clinical Sciences Lund, Lund University and Skåne University Hospital, Lund, Sweden.
Pieter S HiemstraDepartment of Pulmonology, Leiden University Medical Center, Leiden, The Netherlands.ORCID http://orcid.org/0000-0002-0238-5982
Arne EgestenRespiratory Medicine & Allergology, Department of Clinical Sciences Lund, Lund University and Skåne University Hospital, Lund, Sweden.
Lund University · SELeiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteopontin (OPN) plays a role in inflammation via recruitment of neutrophils and tissue remodeling. In this study, we investigated the distribution of OPN-expressing cells in the airway epithelium of normal lung tissue and that from patients with chronic obstructive pulmonary disease (COPD). OPN was detected on the epithelial cell surface of small airways and in scattered cells within the epithelial cell layer. Staining revealed higher OPN concentrations in tissue showing moderate to severe COPD compared to that in controls. In addition, OPN expression was confined to goblet and club cells, and was absent from ciliated and basal cells as detected via immunohistochemistry. However, OPN expression was up-regulated in submerged basal cells cultures exposed to cigarette smoke (CS) extract. Cell fractioning of air-liquid interface cultures revealed increased OPN production from basal compartment cells compared to that in luminal fraction cells. Furthermore, both constitutive and CS-induced expression of OPN decreased during differentiation. In contrast, cultures stimulated with interleukin (IL)-13 to promote goblet cell hyperplasia showed increased OPN production in response to CS exposure. These results indicate that the cellular composition of the airway epithelium plays an important role in OPN expression and that these levels may reflect disease endotypes in COPD.

Indexed as

AdultAirway ObstructionAirway RemodelingCell DifferentiationCells, CulturedCigarette SmokingEpithelial CellsFemaleGene Expression RegulationHumansInflammationInterleukin-13LungMaleNeutrophilsOsteopontinInterleukin-13OsteopontinSmoke

Identifiers

PMID31664154
PMCPMC6820743
OpenAlexW2982504048

What OpenQuestion holds

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LicenceCC BY
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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.