Evidence map›Paper›PMID 22170488›Full record

ArticleThe Journal of investigative dermatology2012

Aldo-keto reductase 1C3 is expressed in differentiated human epidermis, affects keratinocyte differentiation, and is upregulated in atopic dermatitis.

Alon Mantel, Amanda B Carpenter-Mendini, Joanne B Vanbuskirk, Anna De Benedetto, Lisa A Beck, Alice P Pentland

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  10. Leishmania braziliensis prostaglandin FParasites & vectors · 2020
    Article
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  13. Article
  14. Knockdown of AKR1C3 exposes a potential epigenetic susceptibility in prostate cancer cells.The Journal of steroid biochemistry and molecular biology · 2016
    Article
  15. Article
  16. A new target for squamous cell skin cancer?Experimental dermatology · 2015
    Article
  17. Filaggrin silencing by shRNA directly impairs the skin barrier function of normal human epidermal keratinocytes and then induces an immune response.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2015
    Article
  18. Article
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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

6 authors at 1 institution in 1 country.

Alon MantelDepartment of Dermatology, University of Rochester, Rochester, New York 14642, USA.
Amanda B Carpenter-Mendini
Joanne B Vanbuskirk
Anna De Benedetto
Lisa A Beck
Alice P Pentland
University of Rochester · US

Funding

UNIVERSITY OF ROCHESTER'S RESEARCH ASSOCIATE ORGANIZATIONUL1RR024160 · NCRR · UNIVERSITY OF ROCHESTER · PI PEARSON, THOMAS ARTHUR · 2006 to 2011
$38.7M
PGE2 Receptor Function in SkinR01CA117821 · NCI · UNIVERSITY OF ROCHESTER · PI PENTLAND, ALICE P · 2006 to 2010
$1.4M
NCI NIH HHS 5 RO1CA117821NCI NIH HHS R01 CA117821NCRR NIH HHS UL1 RR024160
6 · The paper itself

Abstract

Aldo-keto reductase 1C3 (AKR1C3) has been shown to mediate the metabolism of sex hormones and prostaglandin D(2) (PGD(2)), a lipid mediator that promotes skin inflammation in atopic dermatitis (AD). As both have a role in skin function and pathology, we first sought to investigate the expression pattern of AKR1C3 in normal human epidermis. Immunofluorescence revealed a strong expression of AKR1C3 in the differentiated suprabasal layers compared with the basal layer. Western blot analysis and quantitative PCR confirmed that AKR1C3 expression was also upregulated in differentiation-induced primary human keratinocytes (PHKs). To investigate the functional role of AKR1C3 during PHK differentiation, its expression and activity (measured as PGD(2) reduction to 9α,11β-PGF(2) by ELISA) were impaired by small interfering RNA or 2'-hydroxyflavanone, respectively. Cytokeratin 10 (K10) and loricrin expression were then examined by western blot analysis, thus revealing altered expression of these differentiation markers. Finally, following an observation that the AD-associated mediator, PGD(2), upregulated AKR1C3 expression in PHKs, we used immunofluorescence to examine AKR1C3 expression in AD and psoriasis lesions. AKR1C3 was found to be upregulated in AD but not in psoriasis lesions compared with non-lesional skin. Our work demonstrates a function for AKR1C3 in differentiation-associated gene regulation and also suggests a role in supporting inflammation in AD.

Indexed as

3-Hydroxysteroid DehydrogenasesAldo-Keto Reductase Family 1 Member C3BiomarkersCalciumCell DifferentiationCells, CulturedDermatitis, AtopicEpidermal CellsEpidermisFlavanonesGene Expression RegulationHumansHydroxyprostaglandin DehydrogenasesKeratin-10KeratinocytesMembrane Proteins2'-hydroxyflavanone3-Hydroxysteroid DehydrogenasesAKR1C3 protein, humanAldo-Keto Reductase Family 1 Member C3BiomarkersCalciumFlavanonesHydroxyprostaglandin DehydrogenasesKeratin-10loricrinMembrane ProteinsProstaglandin D2RNA, Small Interfering

Identifiers

PMID22170488
PMCPMC3305848
OpenAlexW2004682457

What OpenQuestion holds

Textmetadata
LicenceTDM
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.