Evidence map›Paper›PMID 34195593›Full record

ArticleMatrix biology plus2021

Extracellular matrix remodeling associated with bleomycin-induced lung injury supports pericyte-to-myofibroblast transition.

Riley T Hannan, Andrew E Miller, Ruei-Chun Hung, Catherine Sano, Shayn M Peirce, Thomas H Barker

Open access · goldAbstract read
In one paragraph

Article in Matrix biology plus, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  11. Understanding myofibroblast origin in the fibrotic lung.Chinese medical journal pulmonary and critical care medicine · 2024
    Review
  12. Local, Quantitative Morphometry of Fibroproliferative Lung Injury Using Laminin.American journal of respiratory cell and molecular biology · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Lung pericytes as mediators of inflammation.American journal of physiology. Lung cellular and molecular physiology · 2023
    Review
  17. Article
  18. Article
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

Riley T HannanDepartment of Pathology, University of Virginia, 415 Lane Road, Charlottesville, VA, United States.
Andrew E MillerDepartment of Biomedical Engineering, University of Virginia, 415 Lane Road, Charlottesville, VA, United States.
Ruei-Chun HungDepartment of Biomedical Engineering, University of Virginia, 415 Lane Road, Charlottesville, VA, United States.
Catherine SanoDepartment of Chemical Engineering, University of Virginia, 102 Engineer's Way, Charlottesville, VA, United States.
Shayn M PeirceDepartment of Biomedical Engineering, University of Virginia, 415 Lane Road, Charlottesville, VA, United States.
Thomas H BarkerDepartment of Biomedical Engineering, University of Virginia, 415 Lane Road, Charlottesville, VA, United States.
University of Virginia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Of the many origins of pulmonary myofibroblasts, microvascular pericytes are a known source. Prior literature has established the ability of pericytes to transition into myofibroblasts, but provide limited insight into molecular cues that drive this process during lung injury repair and fibrosis. Fibronectin and RGD-binding integrins have long been considered pro-fibrotic factors in myofibroblast biology, and here we test the hypothesis that these known myofibroblast cues coordinate pericyte-to-myofibroblast transitions. Specifically, we hypothesized that αvβ3 integrin engagement on fibronectin induces pericyte transition into myofibroblastic phenotypes in the murine bleomycin lung injury model. Myosin Heavy Chain 11 (Myh11)-CreERT2 lineage tracing in transgenic mice allows identification of cells of pericyte origin and provides a robust tool for isolating pericytes from tissues for further evaluation. We used this murine model to track and characterize pericyte behaviors during tissue repair. The majority of Myh11 lineage-positive cells are positive for the pericyte surface markers, PDGFRβ (55%) and CD146 (69%), and display typical pericyte morphology with spatial apposition to microvascular networks. After intratracheal bleomycin treatment of mice, Myh11 lineage-positive cells showed significantly increased contractile and secretory markers, as well as αv integrin expression. According to RNASeq measurements, many disease and tissue-remodeling genesets were upregulated in Myh11 lineage-positive cells in response to bleomycin-induced lung injury.

Indexed as

BleomycinDifferentiationECM, extracellular matrixIntegrinMyofibroblastPericyteSMC, Smooth muscle cellαSMA, Alpha smooth muscle actin

Identifiers

PMID34195593
PMCPMC8233458
OpenAlexW3117195824

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.