Evidence map›Paper›PMID 23814491›Full record

ArticleNeoplasia (New York, N.Y.)2013

Prostaglandin E2 Promotes UV radiation-induced immune suppression through DNA hypermethylation.

Ram Prasad, Santosh K Katiyar

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.9field-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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Prostaglandin EEXCLI journal · 2025
    Review
  4. Article
  5. Restorative Effect of MicroalgaeInternational journal of molecular sciences · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Anticancer mechanisms of phytochemical compounds: focusing on epigenetic targets.Environmental science and pollution research international · 2021
    Review
  10. Article
  11. ASA Suppresses PGEPharmaceuticals (Basel, Switzerland) · 2020
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. 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

2 authors at 2 institutions in 1 country.

Ram PrasadDepartment of Dermatology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Santosh K Katiyar
Birmingham VA Medical Center · USUniversity of Alabama at Birmingham · US

Funding

Prevention of UV-carcinogenesis through DNA repair-dependent immunomodulationR01CA140197 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KATIYAR, SANTOSH KUMAR, XU, HUI · 2010 to 2014
$1.4M
Prevention of skin cancer by green tea polyphenolsR01AT002536 · NCCIH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KATIYAR, SANTOSH KUMAR · 2006 to 2009
$1.1M
Prevention of photocarcinogenesis by dietary immunomodulationI01BX001410 · VA · BIRMINGHAM VA MEDICAL CENTER · PI KATIYAR, SANTOSH KUMAR · 2012 to 2015
–
BLRD VA I01 BX001410NCCIH NIH HHS AT002536NCCIH NIH HHS R01 AT002536NCI NIH HHS CA140197NCI NIH HHS R01 CA140197
6 · The paper itself

Abstract

Exposure of mice to UV radiation results in suppression of the contact hypersensitivity (CHS) response. Here, we report that the UV-induced suppression of CHS is associated with increases in the levels of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and PGE2 receptors in the exposed skin. UV radiation-induced suppression of CHS was inhibited by topical treatment of the skin with celecoxib or indomethacin (inhibitors of COX-2) or AH6809 (an EP2 antagonist). Moreover, mice deficient in COX-2 were found to be resistant to UV-induced suppression of CHS. The exposure of wild-typemice to UVB radiation resulted in DNA hypermethylation, increased DNA methyltransferase (Dnmt) activity, and elevated levels of Dnmt1, Dnmt3a, and Dnmt3b proteins in the skin, and these responses were downregulated on topical treatment of the site of exposure after irradiation with indomethacin or EP2 antagonist. Topical treatment of UVB-exposed COX-2-deficient mice with PGE2 enhanced the UVB-induced suppression of CHS as well as global DNA methylation and elevated the levels of Dnmt activity and Dnmt proteins in the skin. Intraperitoneal injection of 5-aza-2'-deoxycytidine (5-Aza-dc), a DNA demethylating agent, restored the CHS response to 2,4-dinitrofluorobenzene in UVB-exposed skin and this was associated with the reduction in global DNA methylation and Dnmt activity and reduced levels of Dnmt proteins. Furthermore, treatment with 5-Aza-dc reversed the effect of PGE2 on UV-induced suppression of CHS in COX-2-deficient mice. These findings reveal a previously unrecognized role for PGE2 in the promotion of UVB-induced immunosuppression and indicate that it is mediated through PGE2 regulation of DNA methylation.

Indexed as

DNA MethylationAnimalsAzacitidineCyclooxygenase 2Cyclooxygenase 2 InhibitorsDermatitis, ContactDinoprostoneDisease Models, AnimalDNA (Cytosine-5-)-MethyltransferasesEnzyme ActivationFemaleGene Expression RegulationImmune ToleranceMaleMiceMice, KnockoutAzacitidineCyclooxygenase 2Cyclooxygenase 2 InhibitorsDinoprostoneDNA (Cytosine-5-)-MethyltransferasesReceptors, Prostaglandin E, EP2 SubtypeSp1 Transcription FactorSp3 Transcription Factor

Identifiers

PMID23814491
PMCPMC3689242
OpenAlexW1940279666

What OpenQuestion holds

Textmetadata
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.