Evidence map›Paper›PMID 28005397›Full record

ArticleAmerican journal of respiratory cell and molecular biology2017

Tensin 1 Is Essential for Myofibroblast Differentiation and Extracellular Matrix Formation.

Ksenija Bernau, Elizabeth E Torr, Michael D Evans, Jason K Aoki, Caitlyn R Ngam, Nathan Sandbo

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

46 citing papers in PubMed, 67 citations in OpenAlex.

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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.

Ksenija Bernau1 Department of Medicine and.
Elizabeth E Torr1 Department of Medicine and.
Michael D Evans2 Biostatistics and Medical Informatics, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, Wisconsin.
Jason K Aoki1 Department of Medicine and.
Caitlyn R Ngam1 Department of Medicine and.
Nathan Sandbo1 Department of Medicine and.ORCID 0000-0002-5732-4589
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
TNS1 in cell-matrix interactions and pulmonary fibrosisR03HL136795 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI SANDBO, NATHAN K · 2017 to 2018
$153k
NCI NIH HHS P30 CA014520NHLBI NIH HHS K08 HL093367NHLBI NIH HHS R03 HL136795
6 · The paper itself

Abstract

Myofibroblasts, the primary effector cells that mediate matrix remodeling during pulmonary fibrosis, rapidly assemble an extracellular fibronectin matrix. Tensin (TNS) 1 is a key component of specialized cellular adhesions (fibrillar adhesions) that bind to extracellular fibronectin fibrils. We hypothesized that TNS1 may play a role in modulating myofibroblast-mediated matrix formation. We found that TNS1 expression is increased in fibroblastic foci from lungs with idiopathic pulmonary fibrosis. Transforming growth factor (TGF)-β profoundly up-regulates TNS1 expression with kinetics that parallel the expression of the myofibroblast marker, smooth muscle α-actin. TGF-β-induced TNS1 expression is dependent on signaling through the TGF-β receptor 1 and is Rho coiled-coiled kinase/actin/megakaryoblastic leukemia-1/serum response factor dependent. Small interfering RNA-mediated knockdown of TNS1 disrupted TGF-β-induced myofibroblast differentiation, without affecting TGF-β/Smad signaling. In contrast, loss of TNS1 resulted in disruption of focal adhesion kinase phosphorylation, focal adhesion formation, and actin stress fiber development. Finally, TNS1 was essential for the formation of fibrillar adhesions and the assembly of nascent fibronectin and collagen matrix in myofibroblasts. In summary, our data show that TNS1 is a novel megakaryoblastic leukemia-1-dependent gene that is induced during pulmonary fibrosis. TNS1 plays an essential role in TGF-β-induced myofibroblast differentiation and myofibroblast-mediated formation of extracellular fibronectin and collagen matrix. Targeted disruption of TNS1 and associated signaling may provide an avenue to inhibit tissue fibrosis.

Indexed as

Cell DifferentiationActinsExtracellular MatrixFocal AdhesionsHumansMAP Kinase Kinase KinasesMyofibroblastsPolymerizationProtein Serine-Threonine KinasesPulmonary FibrosisReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type Irho-Associated KinasesSignal TransductionSmad ProteinsTensinsActinsMAP3K9 protein, humanMAP Kinase Kinase KinasesProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type Irho-Associated KinasesSmad ProteinsTensinsTransforming Growth Factor betaextracellular matrixfibrillar adhesionmegakaryoblastic leukemia-1myofibroblasttensin 1

Identifiers

PMID28005397
PMCPMC5449508
OpenAlexW2564086068

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.