Evidence map›Paper›PMID 23844043›Full record

ArticlePloS one2013

UVB irradiation regulates ERK1/2- and p53-dependent thrombomodulin expression in human keratinocytes.

Huey-Chun Huang, Tsong-Min Chang, Yu-Jia Chang, Hsin-Yun Wen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Modeling of the Senescence-Associated Phenotype in Human Skin Fibroblasts.International journal of molecular sciences · 2022
    Article
  2. The Role of microRNAs in Organismal and Skin Aging.International journal of molecular sciences · 2020
    Review
  3. Effects of Saccharides from Arctium lappa L. Root on FeClOxidative medicine and cellular longevity · 2020
    Article
  4. Thrombomodulin Regulation of Mitogen-Activated Protein Kinases.International journal of molecular sciences · 2019
    Review
  5. Article
  6. Article
  7. Article
  8. Extract fromEvidence-based complementary and alternative medicine : eCAM · 2017
    Article
  9. Review
  10. Article
  11. 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

4 authors at 3 institutions in 2 countries.

Huey-Chun HuangDepartment of Medical Laboratory Science and Biotechnology, College of Health Care, China Medical University, Taichung, Taiwan. lchuang@mail.cmu.edu.tw
Tsong-Min Chang
Yu-Jia Chang
Hsin-Yun Wen
China Medical University · TWHungkuang University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thrombomodulin (TM) is highly expressed in endothelial cells and acts as a natural anticoagulation factor to maintain circulation homeostasis. TM is an interesting molecule with many physiological functions, including anti-inflammation, anti-thrombosis, and carcinogenesis inhibition. TM can also be detected on the spinous layer of epidermal keratinocytes. However, the role of epidermal TM is still under investigation. In this study, we investigated keratinocyte TM expression and regulation in response to sub-cytotoxic ultraviolet B (UVB) irradiation. Oxidative stress was assessed with DCF and the results revealed that UVB irradiation significantly and dose-dependently augmented reactive oxygen species (ROS) production in HaCaT cells. In addition, low-dose UVB irradiation decreased TM mRNA and protein levels. Blocking ROS production and ERK activation prevented UVB-induced TM down-regulation. The nuclear p53 accumulation and TM promoter binding was observed within 3 h after UVB exposure. Small interfering RNA-mediated p53 knockdown disrupted the UVB-mediated TM protein down-regulation. Our study demonstrates that UVB irradiation results in ROS accumulation and ERK activation, which causes the nuclear p53 accumulation and TM promoter binding to inhibit TM expression. This study provides novel evidence demonstrating that p53 serves as a key regulator of keratinocyte TM expression.

Indexed as

Cell LineCell NucleusGene Expression RegulationHumansKeratinocytesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Oxidative StressPromoter Regions, GeneticProtein BindingReactive Oxygen SpeciesRNA, Small InterferingSignal TransductionThrombomodulinTumor Suppressor Protein p53Ultraviolet RaysMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Reactive Oxygen SpeciesRNA, Small InterferingTHBD protein, humanThrombomodulinTumor Suppressor Protein p53

Identifiers

PMID23844043
PMCPMC3699658
OpenAlexW2049961080

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.