Evidence map›Paper›PMID 31916038›Full record

ArticleJournal of gastroenterology2020

Sodium absorption stimulator prostasin (PRSS8) has an anti-inflammatory effect via downregulation of TLR4 signaling in inflammatory bowel disease.

Yoshihiko Sugitani, Atsushi Nishida, Osamu Inatomi, Masashi Ohno, Takayuki Imai, Masahiro Kawahara, Kenichiro Kitamura, Akira Andoh

Abstract read
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In one paragraph

Article in Journal of gastroenterology, 2020. 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
1.8field-weighted citation impact, top 15% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

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  8. ENaC activation by proteases.Acta physiologica (Oxford, England) · 2022
    Review
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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

8 authors at 2 institutions in 1 country.

Yoshihiko SugitaniDepartment of Medicine, Shiga University of Medical Science, Seta Tsukinowa, Otsu, 520-2192, Japan.
Atsushi NishidaDepartment of Medicine, Shiga University of Medical Science, Seta Tsukinowa, Otsu, 520-2192, Japan.
Osamu InatomiDepartment of Medicine, Shiga University of Medical Science, Seta Tsukinowa, Otsu, 520-2192, Japan.
Masashi OhnoDepartment of Medicine, Shiga University of Medical Science, Seta Tsukinowa, Otsu, 520-2192, Japan.
Takayuki ImaiDepartment of Medicine, Shiga University of Medical Science, Seta Tsukinowa, Otsu, 520-2192, Japan.
Masahiro KawaharaDepartment of Medicine, Shiga University of Medical Science, Seta Tsukinowa, Otsu, 520-2192, Japan.
Kenichiro KitamuraThird Department of Internal Medicine, Faculty of Medicine, University of Yamanashi, 1110, Shimokato, Chuo, Yamanashi, 409-3898, Japan.
Akira AndohDepartment of Medicine, Shiga University of Medical Science, Seta Tsukinowa, Otsu, 520-2192, Japan. andoh@belle.shiga-med.ac.jp.ORCID http://orcid.org/0000-0001-8533-2669
Shiga University of Medical Science · JPUniversity of Yamanashi Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProstasin (PRSS8) is a stimulator of epithelial sodium transport. In this study, we evaluated alteration of prostasin expression in the inflamed mucosa of patients with inflammatory bowel disease (IBD) and investigated the role of prostasin in the gut inflammation.

methodsProstasin expression was evaluated by immunohistochemical staining. Dextran sodium sulfate (DSS)-colitis was induced in mice lacking prostasin specifically in intestinal epithelial cells (PRSS8

resultsIn colonic mucosa of healthy individuals, prostasin was strongly expressed at the apical surfaces of epithelial cells, and this was markedly decreased in active mucosa of both ulcerative colitis and Crohn's disease. DSS-colitis was exacerbated in PRSS8

conclusionProstasin has an anti-inflammatory effect via downregulation of TLR4 expression in colonic epithelial cells. Reduced prostasin expression in IBD mucosa is linked to the deterioration of local anti-inflammatory activity and may contribute to the persistence of mucosal inflammation.

Indexed as

AnimalsColitisColitis, UlcerativeColonCrohn DiseaseDextran SulfateDown-RegulationEpithelial CellsFemaleGene ExpressionGene SilencingHT29 CellsHumansIntestinal MucosaMiceMice, KnockoutDextran SulfateNF-kappa BProstasinRNA, MessengerSerine EndopeptidasesTight Junction ProteinsTLR4 protein, humanToll-Like Receptor 4Mucosal permeabilityNF-κBProstasinTLR4

Identifiers

PMID31916038
OpenAlexW3000149939

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.