Evidence map›Paper›PMID 20722056›Full record

ArticleInflammatory bowel diseases2011

Cytokine regulation of OCTN2 expression and activity in small and large intestine.

Mikihiro Fujiya, Yuhei Inaba, Mark W Musch, Shien Hu, Yutaka Kohgo, Eugene B Chang

Open access · bronzeAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 28% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  10. Host-microbiome interaction in Crohn's disease: A familiar or familial issue?World journal of gastrointestinal pathophysiology · 2015
    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

6 authors at 2 institutions in 2 countries.

Mikihiro FujiyaDepartment of Gastroenterology, Asahikawa Medical School, Asahikawa, Japan.
Yuhei Inaba
Mark W Musch
Shien Hu
Yutaka Kohgo
Eugene B Chang
University of Chicago · USAsahikawa Medical University · JP

Funding

ULTRASTRUCTURE AND CYTOMORPHOLOGY COREP30DK042086 · NIDDK · UNIVERSITY OF CHICAGO · PI LIU, CAMBRIAN YANGSHAO · 1990 to 2025
$29.8M
Mutualistic relationship between Hsp25/27 and gut microbes as a major and essential determinant of mucosal healing and microbial fitness following intestinal injuryR01DK047722 · NIDDK · UNIVERSITY OF CHICAGO · PI CHANG, EUGENE B · 1993 to 2020
$4.3M
Cytoprotective Role of Heat Shock Proteins in IBDR37DK047722 · NIDDK · UNIVERSITY OF CHICAGO · PI CHANG, EUGENE B · 2008 to 2017
$3.8M
NIDDK NIH HHS DK-42086NIDDK NIH HHS DK-47722NIDDK NIH HHS P30 DK042086NIDDK NIH HHS R01 DK047722NIDDK NIH HHS R37 DK047722
6 · The paper itself

Abstract

backgroundThe organic cation transporter OCTN2 is located on the IBD5 risk allele and has been implicated in the pathogenesis of inflammatory bowel diseases (IBD). OCTN2 is expressed in the apical membrane and transports many solutes including bacteria-derived mediators that may be involved in host-microbial interactions. To explore its role further, we examined potential regulatory factors in human IBD and in experimental models of OCTN2 expression.

methodsHuman colonic epithelial cells (Caco2BBE) were used to investigate the effects of inflammatory mediators on OCTN2 activity and expression. Apical membrane expression of OCTN2 was assessed by surface biotinylation. Rag-1(-/-) -deficient mice were used to determine the potential role of adaptive immune cells in the regulation of OCTN2 expression. C57Bl/6 mice were treated with the cytokines interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) to determine the effects on OCTN2 expression and activity. OCTN2 expression in human IBD specimens was assessed by Western blotting and immunohistochemistry.

resultsOCTN2 activity and expression are regulated by the state of intestinal inflammation. OCTN2 expression in colonic tissues of Rag-1(-/-) -deficient mice was reduced. Treatment with IFN-γ and TNF-α increased intestinal OCTN2 expression, particularly in the colon. IFN-γ increased both total and apical membrane expression of Caco2BBE OCTN2, whereas TNF-α stimulated apical expression. Colonic epithelial OCTN2 expression was increased in actively inflamed areas of both Crohn's disease and ulcerative colitis.

conclusionsIntestinal epithelial OCTN2 expression is increased by intestinal inflammation, most likely through increased levels of proinflammatory cytokines. These findings suggest that OCTN2 may participate to restoration of intestinal homeostasis under conditions of inflammation-associated stress.

Indexed as

AnimalsBlotting, WesternCells, CulturedColonCrohn DiseaseCytokinesEpithelial CellsHomeodomain ProteinsHumansImmunoenzyme TechniquesIntestine, LargeIntestine, SmallMiceMice, Inbred C57BLOrganic Cation Transport ProteinsReverse Transcriptase Polymerase Chain ReactionCytokinesHomeodomain ProteinsOrganic Cation Transport ProteinsRAG-1 proteinRNA, MessengerRNA, Small InterferingSLC22A5 protein, humanSlc22a5 protein, mouseSolute Carrier Family 22 Member 5

Identifiers

PMID20722056
PMCPMC2990793
OpenAlexW2061694489

What OpenQuestion holds

Textmetadata
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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.