Evidence map›Paper›PMID 25627685›Full record

ArticleThe Journal of biological chemistry2015

Myofibroblasts exhibit enhanced fibronectin assembly that is intrinsic to their contractile phenotype.

Elizabeth E Torr, Caitlyn R Ngam, Ksenija Bernau, Bianca Tomasini-Johansson, Benjamin Acton, Nathan Sandbo

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 77 citations in OpenAlex.

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  10. Anoctamin-1 is induced by TGF-β and contributes to lung myofibroblast differentiation.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  11. Article
  12. Fibronectin-targeted FUD and PEGylated FUD peptides for fibrotic diseases.Journal of controlled release : official journal of the Controlled Release Society · 2023
    Article
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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

6 authors at 1 institution in 1 country.

Elizabeth E TorrFrom the Departments of Medicine and.
Caitlyn R NgamFrom the Departments of Medicine and.
Ksenija BernauFrom the Departments of Medicine and.
Bianca Tomasini-JohanssonSurgery, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, Wisconsin 53792.
Benjamin ActonFrom the Departments of Medicine and.
Nathan SandboFrom the Departments of Medicine and nsandbo@medicine.wisc.edu.
University of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
Signaling Pathways Regulating Serum Response Factor in Pulmonary FibrosisK08HL093367 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI SANDBO, NATHAN K · 2009 to 2013
$621k
NCI NIH HHS P30 CA014520NHLBI NIH HHS 5K08HL093367NHLBI NIH HHS K08 HL093367
6 · The paper itself

Abstract

Myofibroblasts have increased expression of contractile proteins and display augmented contractility. It is not known if the augmented contractile gene expression characterizing the myofibroblast phenotype impacts its intrinsic ability to assemble fibronectin (FN) and extracellular matrix. In this study we investigated whether myofibroblasts displayed increased rates of FN fibril assembly when compared with their undifferentiated counterparts. Freshly plated myofibroblasts assemble exogenous FN (488-FN) into a fibrillar matrix more rapidly than fibroblasts that have not undergone myofibroblast differentiation. The augmented rate of FN matrix formation by myofibroblasts was dependent on intact Rho/Rho kinase (ROCK) and myosin signals inasmuch as treatment with Y27632 or blebbistatin attenuated 488-FN assembly. Inhibiting contractile gene expression by pharmacologic disruption of the transcription factors megakaryoblastic leukemia-1 (MKL1)/serum response factor (SRF) during myofibroblast differentiation resulted in decreased contractile force generation and attenuated 488-FN incorporation although not FN expression. Furthermore, disruption of the MKL1/SRF target gene, smooth muscle α-actin (α-SMA) via siRNA knockdown resulted in attenuation of 488-FN assembly. In conclusion, this study demonstrates a linkage between increased contractile gene expression, most importantly α-SMA, and the intrinsic capacity of myofibroblasts to assemble exogenous FN into fibrillar extracellular matrix.

Indexed as

ActinsCell DifferentiationCells, CulturedExtracellular MatrixFibroblastsFibronectinsHumansMyofibroblastsPulmonary FibrosisSerum Response FactorTrans-ActivatorsTransforming Growth Factor betaActinsFibronectinsMRTFA protein, humanSerum Response FactorTrans-ActivatorsTransforming Growth Factor betaExtracellular MatrixFibroblastFibronectinMegakaryoblastic Leukemia-1MyofibroblastSerum Response FactorSmooth Muscle α-ActinTransforming Growth Factor β (TGF-B)

Identifiers

PMID25627685
PMCPMC4358119
OpenAlexW1988665049

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.