Evidence map›Paper›PMID 18832581›Full record

ArticleThe American journal of pathology2008

Transforming growth factor-beta regulates in vitro heart valve repair by activated valve interstitial cells.

Amber C Liu, Avrum I Gotlieb

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 102 citations in OpenAlex.

  1. Review
  2. Valve biology and rheumatic heart disease pathogenesis.Nature cardiovascular research · 2026
    Review
  3. Review
  4. Article
  5. Network modeling predicts personalized gene expression and drug responses in valve myofibroblasts cultured with patient sera.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Tumor necrosis factor-α promotes and exacerbates calcification in heart valve myofibroblast populations.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
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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

2 authors at 1 institution in 1 country.

Amber C LiuDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Ontario, Canada.
Avrum I Gotlieb
University of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The regulation of valve interstitial cell (VIC) function in response to tissue injury and valve disease is not well understood. Because transforming growth factor-beta (TGF-beta) has been implicated in tissue repair, we tested the hypothesis that TGF-beta is a regulator of VIC activation and associated cell responses that occur during early repair processes. We used a well-characterized wound model that was created by mechanical denudation of a confluent VIC monolayer to study activation and repair 24 hours after wounding. VIC activation was demonstrated by immunofluorescent localization of alpha-smooth muscle actin (alpha-SMA), and alpha-SMA mRNA levels were quantified by real-time polymerase chain reaction. Proliferation and apoptosis were quantified by bromodeoxyuridine staining and terminal deoxynucleotidyl transferase dUTP nick end labeling, respectively. Repair was quantified by measuring VIC extension into the wound, and TGF-beta expression was shown by immunofluorescent localization of intracellular TGF-beta. Compared with nonwounded monolayers, VICs at the wound edge showed alpha-SMA staining, increased alpha-SMA mRNA content, elongation into the wound with stress fibers, proliferation, and apoptosis. VICs at the wound edge also showed increased TGF-beta and pSmad2/3 staining with co-expression of alpha-SMA. Addition of TGF-beta neutralizing antibody to the wound decreased VIC activation, alpha-SMA mRNA content, proliferation, apoptosis, wound closure rate, and stress fibers. Conversely, exogenous addition of TGF-beta to the wound increased VIC activation, proliferation, wound closure rate, and stress fibers. Thus, wounding activates VICs, and TGF-beta signaling modulates VIC response to injury.

Indexed as

Wound HealingActinsAnimalsAntibodiesApoptosisBromodeoxyuridineCell ProliferationFluorescent Antibody TechniqueGene Expression RegulationHeart ValvesIntracellular SpaceModels, BiologicalNeutralization TestsSignal TransductionStress FibersSwineActinsAntibodiesBromodeoxyuridineTransforming Growth Factor beta

Identifiers

PMID18832581
PMCPMC2570119
OpenAlexW2137551251

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.