Evidence map›Paper›PMID 31968599›Full record

ArticleCells2020

Human Skin Keratinocytes on Sustained TGF-β Stimulation Reveal Partial EMT Features and Weaken Growth Arrest Responses.

Sergio Liarte, Ángel Bernabé-García, Francisco J Nicolás

Abstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Sulfated galactans fromiScience · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Etanercept ameliorates psoriasis progression through regulating high mobility group box 1 pathway.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Perinatal derivatives: How to best characterize their multimodal functionsFrontiers in bioengineering and biotechnology · 2022
    Review
  16. Review
  17. Article
  18. Article
  19. LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte.International journal of molecular sciences · 2021
    Article
  20. 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

3 authors.

Sergio LiarteLaboratorio de Regeneración, Oncología Molecular y TGF-β, IMIB-Arrixaca, El Palmar, 30120 Murcia, Spain.
Ángel Bernabé-GarcíaLaboratorio de Regeneración, Oncología Molecular y TGF-β, IMIB-Arrixaca, El Palmar, 30120 Murcia, Spain.
Francisco J NicolásLaboratorio de Regeneración, Oncología Molecular y TGF-β, IMIB-Arrixaca, El Palmar, 30120 Murcia, Spain.ORCID 0000-0002-3969-1430

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defects in wound closure can be related to the failure of keratinocytes to re-epithelize. Potential mechanisms driving this impairment comprise unbalanced cytokine signaling, including Transforming Growth Factor-β (TFG-β). Although the etiologies of chronic wound development are known, the relevant molecular events are poorly understood. This lack of insight is a consequence of ethical issues, which limit the available evidence to humans. In this work, we have used an in vitro model validated for the study of epidermal physiology and function, the HaCaT cells to provide a description of the impact of sustained exposure to TGF-β. Long term TGF-β1 treatment led to evident changes, HaCaT cells became spindle-shaped and increased in size. This phenotype change involved conformational re-arrangements for actin filaments and E-Cadherin cell-adhesion structures. Surprisingly, the signs of consolidated epithelial-to-mesenchymal transition were absent. At the molecular level, modified gene expression and altered protein contents were found. Non-canonical TGF-β pathway elements did not show relevant changes. However, R-Smads experienced alterations best characterized by decreased Smad3 levels. Functionally, HaCaT cells exposed to TGF-β1 for long periods showed cell-cycle arrest. Yet, the strength of this restraint weakens the longer the treatment, as revealed when challenged by pro-mitogenic factors. The proposed setting might offer a useful framework for future research on the mechanisms driving wound chronification.

Indexed as

Cell Cycle CheckpointsCell ProliferationDown-RegulationEpithelial-Mesenchymal TransitionHaCaT CellsHumansKeratinocytesPhenotypeSignal TransductionSkinSmad3 ProteinTranscription, GeneticTransforming Growth Factor betaSmad3 ProteinSMAD3 protein, humanTransforming Growth Factor betacell proliferationchronic woundsEMTkeratinocytessmadsTGF-β

Identifiers

PMID31968599
PMCPMC7017124

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.