Evidence map›Paper›PMID 39348939›Full record

ArticleLife science alliance2024

TLR3 activation mediates partial epithelial-to-mesenchymal transition in human keratinocytes.

Andrea M Schneider, Robert P Feehan, Mackenzie L Sennett, Carson A Wills, Charlotte Garner, Zhaoyuan Cong, Elizabeth M Billingsley, Alexandra F Flamm, Lisa M Shantz, Amanda M Nelson

Abstract read
In one paragraph

Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

10 authors.

Andrea M SchneiderDepartment of Dermatology, Penn State Health Hershey Medical Center, Hershey, PA, USA.ORCID 0000-0002-9725-4634
Robert P FeehanDepartment of Dermatology, Penn State Health Hershey Medical Center, Hershey, PA, USA.ORCID 0000-0001-5368-1872
Mackenzie L SennettDepartment of Dermatology, Penn State Health Hershey Medical Center, Hershey, PA, USA.ORCID 0000-0003-4964-3835
Carson A WillsDepartment of Pediatrics, Penn State College of Medicine, Hershey, PA, USA.
Charlotte GarnerDepartment of Dermatology, Penn State Health Hershey Medical Center, Hershey, PA, USA.ORCID 0000-0002-0772-6483
Zhaoyuan CongDepartment of Dermatology, Penn State Health Hershey Medical Center, Hershey, PA, USA.
Elizabeth M BillingsleyDepartment of Dermatology, Penn State Health Hershey Medical Center, Hershey, PA, USA.
Alexandra F FlammDepartment of Dermatology, Penn State Health Hershey Medical Center, Hershey, PA, USA.
Lisa M ShantzDepartment of Dermatology, Penn State Health Hershey Medical Center, Hershey, PA, USA.ORCID 0000-0001-8814-4022
Amanda M NelsonDepartment of Dermatology, Penn State Health Hershey Medical Center, Hershey, PA, USA anelson@pennstatehealth.psu.edu.ORCID 0000-0001-6375-8706

Funding

Defining the role of Toll-like receptor 3 in skin homeostasis, injury and neoplasiaK01AR069721 · NIAMS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI NELSON, AMANDA MARIE · 2016 to 2020
$659k
UVB Induced TLR3 Mediated Changes in Keratinocyte PhysiologyF30ES030260 · NIEHS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI SCHNEIDER, ANDREA M · 2019 to 2021
$122k
NIAMS NIH HHS K01 AR069721NIEHS NIH HHS F30 ES030260
6 · The paper itself

Abstract

TLR3 is expressed in human skin and keratinocytes, and given its varied role in skin inflammation, development, and regeneration, we sought to determine the cellular response in normal human keratinocytes to TLR3 activation. We investigated this mechanism by treating primary human keratinocytes with both UVB, an endogenous and physiologic TLR3 activator, and poly(I:C), a synthetic and selective TLR3 ligand. TLR3 activation with either UVB or poly(I:C) altered keratinocyte morphology, coinciding with the key features of epithelial-to-mesenchymal transition: increased epithelial-to-mesenchymal transition gene expression, enhanced migration, and increased invasion properties. These results confirm and extend previous studies demonstrating that in addition to its classical role in the innate immune response, TLR3 signaling also regulates stem cell-like properties and developmental programs.

Indexed as

Cell MovementEpithelial-Mesenchymal TransitionKeratinocytesPoly I-CSignal TransductionToll-Like Receptor 3Cells, CulturedHumansSkinUltraviolet RaysPoly I-CTLR3 protein, humanToll-Like Receptor 3

Identifiers

PMID39348939
PMCPMC11443013

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.