Evidence map›Paper›PMID 20014020›Full record

ArticleInflammatory bowel diseases2010

Elevated IL-13Ralpha2 in intestinal epithelial cells from ulcerative colitis or colorectal cancer initiates MAPK pathway.

Debasmita Mandal, Alan D Levine

RetractedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in Inflammatory bowel diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 19% 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, 46 citations in OpenAlex.

  1. Sensitization of colonic nociceptors by IL-13 is dependent on JAK and p38 MAPK activity.American journal of physiology. Gastrointestinal and liver physiology · 2023
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  15. IL-13 receptor α2 contributes to development of experimental allergic asthma.The Journal of allergy and clinical immunology · 2013
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  19. IBD: of mice and men-shedding new light on IL-13 activity in IBD.Nature reviews. Gastroenterology & hepatology · 2011
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Debasmita MandalDepartment of Pathology, Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-4952, USA.
Alan D Levine
Case Western Reserve University · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MARK R CHANCE · 1987 to 2026
$142.3M
The Extracellular Matrix Inflammatory Bowel DiseaseR01DK054213 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI LEVINE, ALAN DAVID · 1998 to 2010
$2.8M
Mucosal T Cells: Is Tolerance Floating on Lipid RaftsR01AI053188 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI LEVINE, ALAN DAVID · 2003 to 2007
$1.3M
NCI NIH HHS P30 CA043703NCI NIH HHS P30 CA43703NIAID NIH HHS AI-53188NIAID NIH HHS R01 AI053188NIDDK NIH HHS DK-54213NIDDK NIH HHS R01 DK054213
6 · The paper itself

Abstract

backgroundChronic inflammation in ulcerative colitis (UC) is a sizeable risk factor for colorectal cancer (CRC). Interleukin-13 (IL-13) is elevated in the UC mucosa and may induce dysregulated signaling in neighboring intestinal epithelial cells (IECs) and thus function as a tumorogenic cytokine.

methodsExpression of IL-13 receptor chains on IECs obtained from control or chronically inflamed mucosa and colonic tumors was quantified by flow cytometry and immunoblot. IL-13Ralpha1 and IL-13Ralpha2 expression was significantly increased on IEC from UC and CRC patients compared to control and Crohn's disease (CD) subjects. Purified IEC from these subjects and cell lines expressing varying ratios of IL-13Ralpha1 and IL-13Ralpha2 chains were stimulated with IL-13 in vitro to investigate by immunoblot the activation of the signal transducer and activator of transcription 6 (STAT6) and mitogen activated protein kinase (MAPK) signaling pathways.

resultsDespite similarly elevated receptor expression in UC and CRC, IL-13 does not activate the STAT6 or MAPK pathways in UC, while in colonic tumors only the STAT6 pathway is activated. Using neutralizing antibodies and cell lines expressing a range of surface densities for IL-13Ralpha1 and IL-3Ralpha2, we demonstrate that IL-13Ralpha2 serves a dual role, initiating MAPK signaling at low concentrations and as an inhibitory, decoy receptor at high IL-13Ralpha2 to IL-13Ralpha1 ratios.

conclusionsIL-13Ralpha2 is both a decoy receptor and induces MAPK signal transduction, depending on its relative expression and the local concentration of IL-13, which together modulate the balance and intensity of the signaling pathways initiated in UC and CRC.

Indexed as

Antibodies, NeutralizingBlotting, WesternCells, CulturedColitis, UlcerativeColonColorectal NeoplasmsCytokinesFlow CytometryHumansInterleukin-13Interleukin-13 Receptor alpha1 SubunitInterleukin-13 Receptor alpha2 SubunitIntestinal MucosaMitogen-Activated Protein KinasesSignal TransductionSTAT3 Transcription FactorAntibodies, NeutralizingCytokinesInterleukin-13Interleukin-13 Receptor alpha1 SubunitInterleukin-13 Receptor alpha2 SubunitMitogen-Activated Protein KinasesSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID20014020
PMCPMC3417296
OpenAlexW2166098164

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.