Evidence map›Paper›PMID 24043489›Full record

ArticleLung2013

Functional characterization of a porcine emphysema model.

Camilla Sichlau Bruun, Louise Kruse Jensen, Páll Skuli Leifsson, Jens Nielsen, Susanna Cirera, Claus Bøttcher Jørgensen, Henrik Elvang Jensen, Merete Fredholm

Abstract read
PubMed Publisher
In one paragraph

Article in Lung, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Preclinical models of COPD: a state of the art review.The European respiratory journal · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. The porcine innate immune system: an update.Developmental and comparative immunology · 2014
    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

8 authors at 2 institutions in 1 country.

Camilla Sichlau BruunDepartment of Veterinary Clinical and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Grønnegårdsvej 3, 1870, Frederiksberg C, Denmark, cvb@sund.ku.dk.
Louise Kruse Jensen
Páll Skuli Leifsson
Jens Nielsen
Susanna Cirera
Claus Bøttcher Jørgensen
Henrik Elvang Jensen
Merete Fredholm
University of Copenhagen · DKTechnical University of Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung emphysema is a central feature of chronic obstructive pulmonary disease (COPD), a frequent human disease worldwide. Cigarette smoking is the major cause of COPD, but genetic predisposition seems to be an important factor. Mutations in surfactant protein genes have been linked to COPD phenotypes in humans. Also, the catalytic activities of metalloproteinases (MMPs) are central in the pathogenesis of emphysema/COPD. Especially MMP9, but also MMP2, MMP7, and MMP12 seem to be involved in human emphysema. MMP12-/- mice are protected from smoke-induced emphysema. ITGB6-/- mice spontaneously develop age-related lung emphysema due to lack of ITGB6-TGF-β1 regulation of the MMP12 expression.

methodsA mutated pig phenotype characterized by age-related lung emphysema and resembling the ITGB6-/- mouse has been described previously. To investigate the emphysema pathogenesis in this pig model, we examined the expression of MMP2, MMP7, MMP9, MMP12, and TGF-β1 by quantitative PCR (qPCR). In addition, immunohistochemical stainings of the lungs with SP-B, SP-C, MMP9, and MMP12 antibodies were performed. The haematologic/immunologic status of the pigs also was studied.

resultsThe qPCR study showed no difference between pigs with and without emphysema, and no systemic differences were indicated by the haematologic and immunologic studies. However, the immunohistochemical stainings showed an increased expression of MMP9 and MMP12 in older, mutated pigs (with emphysema) compared with normal and young mutated pigs (without emphysema).

conclusionsThe pig model is comparable to human emphysema patients and the ITGB6-/- mouse model with respect to both morphology and functionality.

Indexed as

AnimalsDisease Models, AnimalGenotypeHumansImmunohistochemistryIntegrin beta ChainsLungMatrix Metalloproteinase 12Matrix Metalloproteinase 9MiceMice, KnockoutPhenotypePulmonary Disease, Chronic ObstructivePulmonary EmphysemaPulmonary Surfactant-Associated Protein BPulmonary Surfactant-Associated Protein Cintegrin beta6Integrin beta ChainsMatrix Metalloproteinase 12Matrix Metalloproteinase 9Pulmonary Surfactant-Associated Protein BPulmonary Surfactant-Associated Protein CRNA, MessengerTransforming Growth Factor beta1

Identifiers

PMID24043489
OpenAlexW2049037527

What OpenQuestion holds

Textmetadata
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.