Evidence map›Paper›PMID 24450478›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

Proteoglycans maintain lung stability in an elastase-treated mouse model of emphysema.

Ayuko Takahashi, Arnab Majumdar, Harikrishnan Parameswaran, Erzsébet Bartolák-Suki, Béla Suki

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Chronic lung diseases: entangled in extracellular matrix.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  9. Article
  10. Article
  11. Bioengineering the Blood-gas Barrier.Comprehensive Physiology · 2020
    Review
  12. Article
  13. Article
  14. The consequence of matrix dysfunction on lung immunity and the microbiome in COPD.European respiratory review : an official journal of the European Respiratory Society · 2018
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Matrix Remodeling in Pulmonary Fibrosis and Emphysema.American journal of respiratory cell and molecular biology · 2016
    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

5 authors at 1 institution in 1 country.

Ayuko TakahashiDepartment of Biomedical Engineering, Boston University, Boston, Massachusetts.
Arnab Majumdar
Harikrishnan Parameswaran
Erzsébet Bartolák-Suki
Béla Suki
Boston University · US

Funding

Regulatory roles of variable mechanical stimuli in cell functionR01HL098976 · NHLBI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI SUKI, BELA · 2009 to 2013
$2.3M
Extracellular determinants of airway smooth muscle force: A new paradigm for sustK99HL122513 · NHLBI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI PARAMESWARAN, HARIKRISHNAN · 2014 to 2015
$227k
NHLBI NIH HHS HL-098976NHLBI NIH HHS K99 HL122513NHLBI NIH HHS R01 HL098976
6 · The paper itself

Abstract

Extracellular matrix remodeling and tissue rupture contribute to the progression of emphysema. Lung tissue elasticity is governed by the tensile stiffness of fibers and the compressive stiffness of proteoglycans. It is not known how proteoglycan remodeling affects tissue stability and destruction in emphysema. The objective of this study was to characterize the role of remodeled proteoglycans in alveolar stability and tissue destruction in emphysema. At 30 days after treatment with porcine pancreatic elastase, mouse lung tissue stiffness and alveolar deformation were evaluated under varying tonicity conditions that affect the stiffness of proteoglycans. Proteoglycans were stained and measured in the alveolar walls. Computational models of alveolar stability and rupture incorporating the mechanical properties of fibers and proteoglycans were developed. Although absolute tissue stiffness was only 24% of normal, changes in relative stiffness and alveolar shape distortion due to changes in tonicity were increased in emphysema (P < 0.01 and P < 0.001). Glycosaminoglycan amount per unit alveolar wall length, which is responsible for proteoglycan stiffness, was higher in emphysema (P < 0.001). Versican expression increased in the tissue, but decorin decreased. Our network model predicted that the rate of tissue deterioration locally governed by mechanical forces was reduced when proteoglycan stiffness was increased. Consequently, this general network model explains why increasing proteoglycan deposition protects the alveolar walls from rupture in emphysema. Our results suggest that the loss of proteoglycans observed in human emphysema contributes to disease progression, whereas treatments that promote proteoglycan deposition in the extracellular matrix should slow the progression of emphysema.

Indexed as

Disease Models, AnimalAnimalsBlotting, WesternExtracellular MatrixGlycosaminoglycansHumansImage Processing, Computer-AssistedLungMiceMice, Inbred C57BLPancreatic ElastaseProteoglycansPulmonary AlveoliPulmonary EmphysemaRespiratory MechanicsStress, MechanicalGlycosaminoglycansPancreatic ElastaseProteoglycansalveolar stabilityglycosaminoglycannetwork modeltissue stiffness

Identifiers

PMID24450478
PMCPMC4091854
OpenAlexW2098233799

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.