Evidence map›Paper›PMID 39350252›Full record

ArticleCell communication and signaling : CCS2024

Keratinocyte derived extracellular vesicles mediated crosstalk between epidermis and dermis in UVB-induced skin inflammation.

Yubin Li, Avital Baniel, DeAnna Diaz, Mariko Ogawa-Momohara, Cristina Ricco, Ahmed Eldaboush, Muhammad Bashir, Meena Sharma, Ming-Lin Liu, Victoria P Werth

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Characterizing Keratinocyte-Derived Extracellular Vesicles in UVB-Irradiated Murine Skin.JID innovations : skin science from molecules to population health · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. 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

10 authors.

Yubin Li *Corporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, USA.
Avital Baniel *Corporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, USA.
DeAnna DiazCorporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, USA.
Mariko Ogawa-MomoharaCorporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, USA.
Cristina RiccoCorporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, USA.
Ahmed EldaboushCorporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, USA.
Muhammad BashirCorporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, USA.
Meena SharmaCorporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, USA.
Ming-Lin LiuCorporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, USA.
Victoria P WerthCorporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, USA. Victoria.Werth@pennmedicine.upenn.edu.

Funding

Study Design and Data AnalysisP30AR069589 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI Elizabeth Anne Grice · 2016 to 2026
$8.6M
NIAMS NIH HHS P30 AR069589
6 · The paper itself

Abstract

background and rationaleUltraviolet-B (UVB) light induces dermal inflammation, although it is mostly absorbed in the epidermis. Recent reports suggest extracellular vesicles (EVs) act as a mediator of photodamage signaling. Melatonin is reported to be a protective factor against UV-induced damage. We hypothesized that EVs derived from UVB-irradiated keratinocytes might trigger proinflammatory responses in dermal cells and tested whether melatonin can ameliorate UVB-induced inflammation.

methodsWe used UVB-irradiated HaCaT cells, primary keratinocytes and STING knock-out mice to model production of EVs under photodamaging conditions and performed immunoblotting and ELISA to measure their effect on dermal macrophages.

resultsUVB-irradiated keratinocytes produce an increased number of EVs that contain higher concentrations of DNA and protein compared with controls. KC-derived EVs (KEVs) induced a STING- and inflammasome-mediated proinflammatory response in macrophages in vitro, and a pronounced inflammatory infiltrate in mouse dermis in vivo. Melatonin ameliorated KEVs inflammatory effect both in vitro and in vivo.

conclusionsThis data suggests EVs are mediators in a crosstalk that takes place between keratinocytes and their neighboring cells as a result of photodamage. Further studies exploring EVs induced by damaging doses of UVB, and their impact on other cells will provide insight into photodamage and may help develop targeted therapeutic approaches.

Indexed as

DermisEpidermisExtracellular VesiclesKeratinocytesUltraviolet RaysAnimalsHaCaT CellsHumansInflammationMacrophagesMelatoninMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMelatoninMembrane Proteins

Identifiers

PMID39350252
PMCPMC11441254

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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.