Evidence map›Paper›PMID 32198404›Full record

ArticleScientific reports2020

Tenascin-C inactivation impacts lung structure and function beyond lung development.

Sandrine Gremlich, Matthias Roth-Kleiner, Lucile Equey, Kleanthis Fytianos, Johannes C Schittny, Tiziana P Cremona

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
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  4. A Novel Regulatory Role for RPS4Y1 in Inflammatory and Fibrotic Processes.International journal of molecular sciences · 2025
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  5. Article
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  8. Review
  9. Article
  10. Article
  11. Defining the versican interactome in lung health and disease.American journal of physiology. Cell physiology · 2022
    Review
  12. Response to Hypoxia and the Ensuing Dysregulation of Inflammation ImpactsAmerican journal of respiratory and critical care medicine · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Airway compliance measurements in mouse models of respiratory diseases.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  18. Tenascin-C in Heart Diseases-The Role of Inflammation.International journal of molecular sciences · 2021
    Review
  19. Article
  20. Tenascin-C: Friend or Foe in Lung Aging?Frontiers in physiology · 2021
    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

6 authors at 2 institutions in 1 country.

Sandrine GremlichClinic of Neonatology, Department woman-mother-child, University Hospital and University of Lausanne, Lausanne, Switzerland. sandrine.gremlich-irrausch@chuv.ch.
Matthias Roth-KleinerClinic of Neonatology, Department woman-mother-child, University Hospital and University of Lausanne, Lausanne, Switzerland.
Lucile EqueyClinic of Neonatology, Department woman-mother-child, University Hospital and University of Lausanne, Lausanne, Switzerland.
Kleanthis FytianosDepartment of Bio-medical Research, University of Bern, Bern, Switzerland.
Johannes C SchittnyInstitute of Anatomy, University of Bern, Bern, Switzerland.ORCID http://orcid.org/0000-0003-4025-3961
Tiziana P CremonaInstitute of Anatomy, University of Bern, Bern, Switzerland.
University of Bern · CHUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tenascin-C (TNC) is an extracellular matrix protein expressed at high levels during lung organogenesis. Later, TNC is only transiently de novo expressed to orchestrate tissue repair in pathological situations. We previously showed that TNC inactivation affects lung development and thus evaluated here the implications on lung function in newborn/adult mice. Respiratory function parameters were measured in anesthetized and mechanically ventilated wild-type (WT) and TNC-deficient mice at 5 (P5) and 90 (P90) days of age under basal conditions, as well as following high tidal volume (HTV) ventilation. At P5, TNC-deficient mice showed an increased static compliance (Cst) and inspiratory capacity (IC) relative to WT at baseline and throughout HTV. At P90, however, Cst and IC were only elevated at baseline. Control non-ventilated newborn and adult TNC-deficient mice showed similar lung morphology, but less alpha smooth muscle actin (α-SMA) around small airways. SMA + cells were decreased by 50% in adult TNC-deficient lungs and collagen layer thickened around small airways. Increased surfactant protein C (SP-C) and altered TGFβ and TLR4 signaling pathways were also detected. Thus, TNC inactivation-related defects during organogenesis led to persisting functional impairment in adulthood. This might be of interest in the context of pulmonary diseases with thickened airway smooth muscle layer or ventilation heterogeneity, like asthma and COPD.

Indexed as

ActinsAnimalsCell ProliferationCollagenExtracellular MatrixLungMiceMice, KnockoutOrganogenesisPulmonary Surfactant-Associated Protein CRespiration, ArtificialSignal TransductionTenascinTidal VolumeToll-Like Receptor 4Transforming Growth Factor betaActa2 protein, mouseActinsCollagenPulmonary Surfactant-Associated Protein CTenascinTlr4 protein, mouseTnc protein, mouseToll-Like Receptor 4Transforming Growth Factor beta

Identifiers

PMID32198404
PMCPMC7083919
OpenAlexW3012255302

What OpenQuestion holds

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Registered trials

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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.