Evidence map›Paper›PMID 31358001›Full record

ArticleRespiratory research2019

Anti-fibrotic effects of tannic acid through regulation of a sustained TGF-beta receptor signaling.

Eleanor B Reed, Shawn Ard, Jennifer La, Chan Young Park, Laura Culligan, Jeffrey J Fredberg, Larisa V Smolyaninova, Sergei N Orlov, Bohao Chen, Robert Guzy and 2 more

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-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

14 citing papers in PubMed, 25 citations in OpenAlex.

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  13. Velvet Antler Peptides Reduce ScarringFrontiers in medicine · 2021
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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

12 authors at 3 institutions in 2 countries.

Eleanor B ReedDepartment of Medicine, Section of Pulmonary and Critical Care Medicine, the University of Chicago, 5841 S. Maryland Ave, MC6076, Chicago, IL, 60637, USA.
Shawn ArdDepartment of Medicine, Section of Pulmonary and Critical Care Medicine, the University of Chicago, 5841 S. Maryland Ave, MC6076, Chicago, IL, 60637, USA.
Jennifer LaDepartment of Medicine, Section of Pulmonary and Critical Care Medicine, the University of Chicago, 5841 S. Maryland Ave, MC6076, Chicago, IL, 60637, USA.
Chan Young ParkMolecular and Integrative Physiological Sciences, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Laura CulliganMolecular and Integrative Physiological Sciences, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Jeffrey J FredbergMolecular and Integrative Physiological Sciences, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Larisa V SmolyaninovaLaboratory of Biomembranes, Faculty of Biology, Lomonosov Moscow State University, Moscow, Russian Federation.
Sergei N OrlovLaboratory of Biomembranes, Faculty of Biology, Lomonosov Moscow State University, Moscow, Russian Federation.
Bohao ChenDepartment of Medicine, Section of Pulmonary and Critical Care Medicine, the University of Chicago, 5841 S. Maryland Ave, MC6076, Chicago, IL, 60637, USA.
Robert GuzyDepartment of Medicine, Section of Pulmonary and Critical Care Medicine, the University of Chicago, 5841 S. Maryland Ave, MC6076, Chicago, IL, 60637, USA.
Gökhan M MutluDepartment of Medicine, Section of Pulmonary and Critical Care Medicine, the University of Chicago, 5841 S. Maryland Ave, MC6076, Chicago, IL, 60637, USA.
Nickolai O DulinDepartment of Medicine, Section of Pulmonary and Critical Care Medicine, the University of Chicago, 5841 S. Maryland Ave, MC6076, Chicago, IL, 60637, USA. ndulin@medicine.bsd.uchicago.edu.ORCID http://orcid.org/0000-0001-6096-5822
University of Chicago · USLomonosov Moscow State University · RUSiberian State Medical University · RU

Funding

Physics of collective cellular migration in lung health and diseaseP01HL120839 · NHLBI · HARVARD SCHOOL OF PUBLIC HEALTH · PI FREDBERG, JEFFREY J · 2014 to 2018
$12.2M
Physics of bronchial epithelial unjammingR01HL148152 · NHLBI · HARVARD SCHOOL OF PUBLIC HEALTH · PI FREDBERG, JEFFREY J, PARK, JIN-AH · 2019 to 2022
$2.2M
Control of myofibroblast activation and pulmonary fibrosis by Na/K-ATPaseR56HL127395 · NHLBI · UNIVERSITY OF CHICAGO · PI DULIN, NICKOLAI O · 2015 to 2015
$389k
NHLBI NIH HHS P01 HL120839NHLBI NIH HHS R01 HL148152NHLBI NIH HHS R56 HL127395NIH HHS 1R56HL127395
6 · The paper itself

Abstract

backgroundPulmonary fibrosis is a progressive disease characterized by structural distortion of the lungs. Transforming growth factor-beta (TGF-beta) is a key cytokine implicated in the pathogenesis of pulmonary fibrosis. TGF-beta-induced myofibroblast differentiation characterized by expression of smooth muscle alpha-actin and extracellular matrix proteins is a key process in pathogenesis of fibrotic disease. Tannic acid is a natural polyphenol with diverse applications. In this study, we investigated the effect of tannic acid on myofibroblast differentiation and pulmonary fibrosis in cultured cells and in bleomycin model of the disease.

methodsPrimary cultured human lung fibroblasts (HLF) were used. The relative levels of proteins were determined by Western blotting. HLF contraction was measured by traction microscopy. Bleomycin-induced pulmonary fibrosis in mice was used as the disease model.

resultsTannic acid inhibited TGF-beta-induced expression of collagen-1 and smooth muscle alpha-actin (SMA) as well as force generation by HLF. Tannic acid did not affect initial phosphorylation of Smad2 in response to TGF-beta, but significantly inhibited sustained Smad2 phosphorylation, which we recently described to be critical for TGF-beta-induced myofibroblast differentiation. Accordingly, tannic acid inhibited Smad-dependent gene transcription in response to TGF-beta, as assessed using luciferase reporter for the activity of Smad-binding elements. Finally, in mouse model of bleomycin-induced pulmonary fibrosis, therapeutic application of tannic acid resulted in a significant reduction of lung fibrosis, decrease in collagen-1 content and of Smad2 phosphorylation in the lungs.

conclusionsThis study demonstrates the anti-fibrotic effect of tannic acid in vitro and in vivo through a regulation of sustained Smad2 phosphorylation.

Indexed as

AnimalsAntifibrinolytic AgentsCells, CulturedFibroblastsHumansLungMiceMice, Inbred C57BLPulmonary FibrosisReceptors, Transforming Growth Factor betaSignal TransductionTanninsAntifibrinolytic AgentsReceptors, Transforming Growth Factor betaTanninsMyofibroblastPulmonary fibrosisSmad2Tannic acidTGF-beta

Identifiers

PMID31358001
PMCPMC6664561
OpenAlexW2964470693

What OpenQuestion holds

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Registered trials

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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.