Evidence map›Paper›PMID 24710357›Full record

ArticlePloS one2014

Oncostatin M mediates STAT3-dependent intestinal epithelial restitution via increased cell proliferation, decreased apoptosis and upregulation of SERPIN family members.

Florian Beigel, Matthias Friedrich, Corina Probst, Karl Sotlar, Burkhard Göke, Julia Diegelmann, Stephan Brand

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Florian BeigelDepartment of Medicine II, University-Hospital Munich-Grosshadern, Ludwig-Maximilians-University Munich, Munich, Germany.
Matthias FriedrichDepartment of Medicine II, University-Hospital Munich-Grosshadern, Ludwig-Maximilians-University Munich, Munich, Germany; Clinic for Preventive Dentistry and Parodontology, Ludwig-Maximilians-University Munich, Munich, Germany.
Corina ProbstDepartment of Medicine II, University-Hospital Munich-Grosshadern, Ludwig-Maximilians-University Munich, Munich, Germany.
Karl SotlarInstitute of Pathology, Ludwig-Maximilians-University Munich, Munich, Germany.
Burkhard GökeDepartment of Medicine II, University-Hospital Munich-Grosshadern, Ludwig-Maximilians-University Munich, Munich, Germany.
Julia DiegelmannDepartment of Medicine II, University-Hospital Munich-Grosshadern, Ludwig-Maximilians-University Munich, Munich, Germany; Clinic for Preventive Dentistry and Parodontology, Ludwig-Maximilians-University Munich, Munich, Germany.
Stephan BrandDepartment of Medicine II, University-Hospital Munich-Grosshadern, Ludwig-Maximilians-University Munich, Munich, Germany.
Ludwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveOncostatin M (OSM) is produced by activated T cells, monocytes, and dendritic cells and signals through two distinct receptor complexes consisting of gp130 and LIFR (I) or OSMR-β and gp130 (II), respectively. Aim of this study was to analyze the role of OSM in intestinal epithelial cells (IEC) and intestinal inflammation.

methodsOSM expression and OSM receptor distribution was analyzed by PCR and immunohistochemistry experiments, signal transduction by immunoblotting. Gene expression studies were performed by microarray analysis and RT-PCR. Apoptosis was measured by caspases-3/7 activity. IEC migration and proliferation was studied in wounding and water soluble tetrazolium assays.

resultsThe IEC lines Caco-2, DLD-1, SW480, HCT116 and HT-29 express mRNA for the OSM receptor subunits gp130 and OSMR-β, while only HCT116, HT-29 and DLD-1 cells express LIFR mRNA. OSM binding to its receptor complex activates STAT1, STAT3, ERK-1/2, SAPK/JNK-1/2, and Akt. Microarray analysis revealed 79 genes that were significantly up-regulated (adj.-p ≤ 0.05) by OSM in IEC. Most up-regulated genes belong to the functional categories "immunity and defense" (p = 2.1 × 10(-7)), "apoptosis" (p = 3.7 × 10(-4)) and "JAK/STAT cascade" (p = 3.4 × 10(-6)). Members of the SERPIN gene family were among the most strongly up-regulated genes. OSM significantly increased STAT3- and MEK1-dependent IEC cell proliferation (p<0.05) and wound healing (p = 3.9 × 10(-5)). OSM protein expression was increased in colonic biopsies of patients with active inflammatory bowel disease (IBD).

conclusionsOSM promotes STAT3-dependent intestinal epithelial cell proliferation and wound healing in vitro. Considering the increased OSM expression in colonic biopsy specimens of patients with active IBD, OSM upregulation may modulate a barrier-protective host response in intestinal inflammation. Further in vivo studies are warranted to elucidate the exact role of OSM in intestinal inflammation and the potential of OSM as a drug target in IBD.

Indexed as

ApoptosisCell ProliferationCaco-2 CellsFemaleHumansInflammatory Bowel DiseasesIntestinal MucosaMaleOncostatin MSerpinsSTAT3 Transcription FactorUp-RegulationWound HealingOncostatin MSerpinsSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID24710357
PMCPMC3977870
OpenAlexW1982516973

What OpenQuestion holds

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LicenceCC BY
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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.