Evidence map›Paper›PMID 38279255›Full record

ArticleInternational journal of molecular sciences2024

Endothelial Protein C Receptor and 3K3A-Activated Protein C Protect Mice from Allergic Contact Dermatitis in a Contact Hypersensitivity Model.

Meilang Xue, Christopher J Jackson, Haiyan Lin, Ruilong Zhao, Hai Po H Liang, Hartmut Weiler, John H Griffin, Lyn March

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

8 authors at 3 institutions in 2 countries.

Meilang XueSutton Arthritis Research Laboratory, Kolling Institute, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2065, Australia.ORCID 0000-0002-8563-7216
Christopher J JacksonSutton Arthritis Research Laboratory, Kolling Institute, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2065, Australia.
Haiyan LinSutton Arthritis Research Laboratory, Kolling Institute, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2065, Australia.
Ruilong ZhaoSutton Arthritis Research Laboratory, Kolling Institute, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2065, Australia.ORCID 0000-0002-4610-4898
Hai Po H LiangSutton Arthritis Research Laboratory, Kolling Institute, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2065, Australia.
Hartmut WeilerVersiti Blood Research Institute, Milwaukee, WI 53226, USA.
John H GriffinDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.
Lyn MarchThe Australian Arthritis and Autoimmune Biobank Collaborative (A3BC), Kolling Institute, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2065, Australia.
The University of Sydney · AUMedical College of Wisconsin · USScripps Research Institute · US

Funding

Regulation of Protein C PathwaysR01HL142975 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI GRIFFIN, JOHN H, MOSNIER, LAURENT OLIVIER · 2018 to 2025
$7.3M
NHLBI NIH HHS R01 HL142975
6 · The paper itself

Abstract

Endothelial protein C receptor (EPCR) is a receptor for the natural anti-coagulant activated protein C (aPC). It mediates the anti-inflammatory and barrier-protective functions of aPC through the cleavage of protease-activated receptor (PAR)1/2. Allergic contact dermatitis is a common skin disease characterized by inflammation and defective skin barrier. This study investigated the effect of EPCR and 3K3A-aPC on allergic contact dermatitis using a contact hypersensitivity (CHS) model. CHS was induced using 1-Fluoro-2,4-dinitrobenzene in EPCR-deficient (KO) and matched wild-type mice and mice treated with 3K3A-aPC, a mutant form of aPC with diminished anti-coagulant activity. Changes in clinical and histological features, cytokines, and immune cells were examined. EPCRKO mice displayed more severe CHS, with increased immune cell infiltration in the skin and higher levels of inflammatory cytokines and IgE than wild-type mice. EPCR, aPC, and PAR1/2 were expressed by the skin epidermis, with EPCR presenting almost exclusively in the basal layer. EPCRKO increased the epidermal expression of aPC and PAR1, whereas in CHS, their expression was reduced compared to wild-type mice. 3K3A-aPC reduced CHS severity in wild-type and EPCRKO mice by suppressing immune cell infiltration/activation and inflammatory cytokines. In summary, EPCRKO exacerbated CHS, whereas 3K3A-aPC could reduce the severity of CHS in both EPCRKO and wild-type mice.

Indexed as

Dermatitis, Allergic ContactProtein CRecombinant ProteinsAnimalsCytokinesEndothelial Protein C ReceptorMiceReceptor, PAR-1Signal Transduction3K3A-APC proteinCytokinesEndothelial Protein C ReceptorProtein CReceptor, PAR-1Recombinant Proteinsimmune cellsmutant activated protein Cprotease-activated receptorskin inflammation

Identifiers

PMID38279255
PMCPMC10816322
OpenAlexW4391035155

What OpenQuestion holds

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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.