Evidence map›Paper›PMID 25008089›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014

Roles of transforming growth factor-β1 and OB-cadherin in porcine cardiac valve myofibroblast differentiation.

Huan Wang, Leslie A Leinwand, Kristi S Anseth

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. 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
1.4field-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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. The critical role of LRG1 in pathological fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Cardiac fibrosis.Cardiovascular research · 2021
    Review
  12. Article
  13. Review
  14. Article
  15. Cadherin-11 as a regulator of valve myofibroblast mechanobiology.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

3 authors at 2 institutions in 1 country.

Huan WangDepartment of Chemical and Biological Engineering, Department of Molecular, Cellular and Developmental Biology, BioFrontiers Institute, and.
Leslie A LeinwandDepartment of Molecular, Cellular and Developmental Biology, BioFrontiers Institute, and.
Kristi S AnsethDepartment of Chemical and Biological Engineering, BioFrontiers Institute, and Howard Hughes Medical Institute, University of Colorado, Boulder, Colorado, USA kristi.anseth@colorado.edu.
University of Colorado Boulder · USHoward Hughes Medical Institute · US

Funding

MYOSIN GENE DIVERSITY AND FUNCTIONR01GM029090 · NIGMS · YESHIVA UNIVERSITY · PI Leslie Anne Leinwand · 1985 to 2026
$12.3M
Bioactive Hydrogel Niches for 3D VIC CultureR01HL089260 · NHLBI · UNIVERSITY OF COLORADO · PI ANSETH, KRISTI S. · 2008 to 2011
$1.3M
Howard Hughes Medical InstituteNHLBI NIH HHS R01 HL089260NIGMS NIH HHS R01 GM029090NIGMS NIH HHS R01 GM29090
6 · The paper itself

Abstract

Calcific aortic stenosis is a common disease, and some of its early causes are the activation and differentiation of resident fibroblasts to myofibroblasts in response to transforming growth factor β1 (TGF-β1). The aim of this study was to understand how TGF-β1 and its downstream effector, OB-cadherin [cadherin 11 (CDH11)], regulate porcine myofibroblast phenotypes. Based on whole-genome microarrays, 95 and 107 genes are up- and down-regulated at both the early (8 h) and the late (24 h) time points of TGF-β1 treatment. Gene functions related to cell adhesion, skeletal system development, and extracellular matrix are up-regulated by TGF-β1, whereas oxidation-reduction and steroid metabolic process are down-regulated. Notably, one of the cell adhesion molecules, CDH11, is up-regulated by ∼2-fold through both the Smad2/3 and the ERK pathways elicited by TGF-β1. CDH11 mediates cell-cell contacts in both valvular fibroblasts and myofibroblasts. Knockdown of CDH11 by small interfering RNA increases the myofibroblast phenotype, including an ∼2-fold increase in α-smooth muscle actin (α-SMA) expression and stress fiber formation. In contrast, increased binding of CDH11 through antibody treatment inhibits α-SMA expression. This study presents gene functional changes in response to TGF-β1 at the systems level and supports an inhibitory role of CDH11 in myofibroblast differentiation.

Indexed as

Cell DifferentiationTranscriptomeActinsAnimalsCadherinsGene Expression ProfilingHeart ValvesMyofibroblastsSwineTransforming Growth Factor betaActinsCadherinsosteoblast cadherinTransforming Growth Factor betaaortic valve fibrosisgenome-wide transcriptionα-smooth muscle actin

Identifiers

PMID25008089
PMCPMC4202096
OpenAlexW2058343866

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.