Evidence map›Paper›PMID 25856770›Full record

ArticleInflammatory bowel diseases2015

G Protein-coupled pH-sensing Receptor OGR1 Is a Regulator of Intestinal Inflammation.

Cheryl de Vallière, Yu Wang, Jyrki J Eloranta, Solange Vidal, Ieuan Clay, Marianne R Spalinger, Irina Tcymbarevich, Anne Terhalle, Marie-Gabrielle Ludwig, Thomas Suply and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

52 citing papers in PubMed, 89 citations in OpenAlex.

  1. Review
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  10. Activation of the proton-sensing GPCR, GPR65 on fibroblast-like synoviocytes contributes to inflammatory joint pain.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. Review
  12. Role of pH-sensing receptors in colitis.Pflugers Archiv : European journal of physiology · 2024
    Review
  13. Bicarbonate secretion and acid/base sensing by the intestine.Pflugers Archiv : European journal of physiology · 2024
    Review
  14. 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

17 authors at 5 institutions in 2 countries.

Cheryl de Vallière*Division of Gastroenterology and Hepatology, University Hospital Zürich, Zürich, Switzerland; †Institute of Physiology, University of Zürich, Zürich, Switzerland; ‡Department of Clinical Pharmacology and Toxicology, University Hospital Zürich, Zürich, Switzerland; and §Novartis Institutes for Biomedical Research, Basel, Switzerland.
Yu Wang
Jyrki J Eloranta
Solange Vidal
Ieuan Clay
Marianne R Spalinger
Irina Tcymbarevich
Anne Terhalle
Marie-Gabrielle Ludwig
Thomas Suply
Michael Fried
Gerd A Kullak-Ublick
Isabelle Frey-Wagner
Michael Scharl
Klaus Seuwen
Carsten A Wagner
Gerhard Rogler
University Hospital of Zurich · CHUniversity Psychiatric Hospital · SINovartis (Switzerland) · CHNovartis Institutes for BioMedical ResearchUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA novel family of proton-sensing G protein-coupled receptors, including OGR1, GPR4, and TDAG8, was identified to be important for physiological pH homeostasis and inflammation. Thus, we determined the function of proton-sensing OGR1 in the intestinal mucosa. MTEHODS: OGR1 expression in colonic tissues was investigated in controls and patients with IBD. Expression of OGR1 upon cell activation was studied in the Mono Mac 6 (MM6) cell line and primary human and murine monocytes by real-time PCR. Ogr1 knockout mice were crossbred with Il-10 deficient mice and studied for more than 200 days. Microarray profiling was performed using Ogr1 and Ogr1 (WT) residential peritoneal macrophages.

resultsPatients with IBD expressed higher levels of OGR1 in the mucosa than non-IBD controls. Treatment of MM6 cells with TNF, led to significant upregulation of OGR1 expression, which could be reversed by the presence of NF-κB inhibitors. Kaplan-Meier survival analysis showed a significantly delayed onset and progression of rectal prolapse in female Ogr1/Il-10 mice. These mice displayed significantly less rectal prolapses. Upregulation of gene expression, mediated by OGR1, in response to extracellular acidification in mouse macrophages was enriched for inflammation and immune response, actin cytoskeleton, and cell-adhesion gene pathways.

conclusionsOGR1 expression is induced in cells of human macrophage lineage and primary human monocytes by TNF. NF-κB inhibition reverses the induction of OGR1 expression by TNF. OGR1 deficiency protects from spontaneous inflammation in the Il-10 knockout model. Our data indicate a pathophysiological role for pH-sensing receptor OGR1 during the pathogenesis of mucosal inflammation.

Indexed as

Acid-Base EquilibriumAnimalsCell LineFemaleHumansInflammatory Bowel DiseasesInterleukin-10Intestinal MucosaIntestinesMacrophages, PeritonealMaleMiceMice, KnockoutReceptors, G-Protein-CoupledGPR68 protein, humanGPR68 protein, mouseIL10 protein, mouseInterleukin-10Receptors, G-Protein-Coupled

Identifiers

PMID25856770
PMCPMC4450952
OpenAlexW2029738113

What OpenQuestion holds

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Registered trials

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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.