Evidence map›Paper›PMID 25955532›Full record

ArticlePloS one2015

Increased Expression of TGF-β Signaling Components in a Mouse Model of Fibrosis Induced by Submandibular Gland Duct Ligation.

Lucas T Woods, Jean M Camden, Farid G El-Sayed, Mahmoud G Khalafalla, Michael J Petris, Laurie Erb, Gary A Weisman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

44 citing papers in PubMed, 67 citations in OpenAlex.

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  15. Identifying Fibrogenic Cells Following Salivary Gland Obstructive Injury.bioRxiv : the preprint server for biology · 2023
    Article
  16. Article
  17. Article
  18. Identifying fibrogenic cells following salivary gland obstructive injury.Frontiers in cell and developmental biology · 2023
    Article
  19. Article
  20. Review
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

7 authors at 1 institution in 1 country.

Lucas T WoodsDepartment of Biochemistry, University of Missouri, Columbia, Missouri, United States of America; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, Missouri, United States of America.
Jean M CamdenDepartment of Biochemistry, University of Missouri, Columbia, Missouri, United States of America; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, Missouri, United States of America.
Farid G El-SayedDepartment of Biochemistry, University of Missouri, Columbia, Missouri, United States of America; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, Missouri, United States of America.
Mahmoud G KhalafallaDepartment of Biochemistry, University of Missouri, Columbia, Missouri, United States of America; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, Missouri, United States of America.
Michael J PetrisDepartment of Biochemistry, University of Missouri, Columbia, Missouri, United States of America; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, Missouri, United States of America; Department of Nutritional Sciences and Exercise Physiology, University of Missouri, Columbia, Missouri, United States of America.
Laurie ErbDepartment of Biochemistry, University of Missouri, Columbia, Missouri, United States of America; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, Missouri, United States of America.
Gary A WeismanDepartment of Biochemistry, University of Missouri, Columbia, Missouri, United States of America; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, Missouri, United States of America.
University of Missouri · US

Funding

VIP RECEPTORS AND SUBMANDIBULAR GLAND FUNCTIONR01DE007389 · NIDCR · UNIVERSITY OF MISSOURI-COLUMBIA · PI WEISMAN, GARY ANDREW · 1988 to 2020
$7.6M
Restoring Salivary Gland Function by Reducing Nucleotide-induced InflammationR01DE023342 · NIDCR · UNIVERSITY OF MISSOURI-COLUMBIA · PI WEISMAN, GARY ANDREW · 2014 to 2018
$2.9M
NIDCR NIH HHS R01 DE007389NIDCR NIH HHS R01DE007389NIDCR NIH HHS R01DE0223342NIDCR NIH HHS R01 DE023342
6 · The paper itself

Abstract

Transforming growth factor-β (TGF-β) is a multi-functional cytokine with a well-described role in the regulation of tissue fibrosis and regeneration in the liver, kidney and lung. Submandibular gland (SMG) duct ligation and subsequent deligation in rodents is a classical model for studying salivary gland damage and regeneration. While previous studies suggest that TGF-β may contribute to salivary gland fibrosis, the expression of TGF-β signaling components has not been investigated in relation to mouse SMG duct ligation-induced fibrosis and regeneration following ductal deligation. Following a 7 day SMG duct ligation, TGF-β1 and TGF-β3 were significantly upregulated in the SMG, as were TGF-β receptor 1 and downstream Smad family transcription factors in salivary acinar cells, but not in ductal cells. In acinar cells, duct ligation also led to upregulation of snail, a Smad-activated E-cadherin repressor and regulator of epithelial-mesenchymal transition, whereas in ductal cells upregulation of E-cadherin was observed while snail expression was unchanged. Upregulation of these TGF-β signaling components correlated with upregulation of fibrosis markers collagen 1 and fibronectin, responses that were inhibited by administration of the TGF-β receptor 1 inhibitors SB431542 or GW788388. After SMG regeneration following a 28 day duct deligation, TGF-β signaling components and epithelial-mesenchymal transition markers returned to levels similar to non-ligated controls. The results from this study indicate that increased TGF-β signaling contributes to duct ligation-induced changes in salivary epithelium that correlate with glandular fibrosis. Furthermore, the reversibility of enhanced TGF-β signaling in acinar cells of duct-ligated mouse SMG after deligation indicates that this is an ideal model for studying TGF-β signaling mechanisms in salivary epithelium as well as mechanisms of fibrosis initiation and their resolution.

Indexed as

Acinar CellsAnimalsBenzamidesBiomarkersCadherinsDisease Models, AnimalFibrosisLigationMaleMice, Inbred C57BLProtein IsoformsProtein Serine-Threonine KinasesPyrazolesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IRegeneration4-(4-(3-(pyridin-2-yl)-1H-pyrazol-4-yl)pyridin-2-yl)-N-(tetrahydro-2H-pyran-4-yl)benzamideBenzamidesBiomarkersCadherinsProtein IsoformsProtein Serine-Threonine KinasesPyrazolesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ISmad ProteinsSnail Family Transcription FactorsTranscription FactorsTransforming Growth Factor beta

Identifiers

PMID25955532
PMCPMC4425516
OpenAlexW391037508

What OpenQuestion holds

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LicenceCC BY
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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.