Evidence map›Paper›PMID 25637652›Full record

ArticleGastroenterology2015

Stem cells for murine interstitial cells of cajal suppress cellular immunity and colitis via prostaglandin E2 secretion.

Maneesh Dave, Yujiro Hayashi, Gabriella B Gajdos, Thomas C Smyrk, Phyllis A Svingen, Sergiy M Kvasha, Andrea Lorincz, Haidong Dong, William A Faubion, Tamas Ordog

Open access · bronzeAbstract read
In one paragraph

Article in Gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Cellular and molecular mechanisms underlying aging-related gastric neuromuscular dysfunction.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2025
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4 · The record

Corrections and comments

  • Commented on by
5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Maneesh DaveGastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota.
Yujiro HayashiGastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota; Enteric Neuroscience Program, Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.
Gabriella B GajdosGastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota; Enteric Neuroscience Program, Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.
Thomas C SmyrkDepartment of Pathology, Mayo Clinic, Rochester, Minnesota.
Phyllis A SvingenGastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota.
Sergiy M KvashaGastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota; Enteric Neuroscience Program, Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.
Andrea LorinczGastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota; Enteric Neuroscience Program, Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.
Haidong DongDepartment of Urology, Mayo Clinic, Rochester, Minnesota.
William A FaubionGastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota. Electronic address: faubion.william@mayo.edu.
Tamas OrdogGastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota; Enteric Neuroscience Program, Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota; Center for Individualized Medicine, Mayo Clinic, Rochester, Minnesota. Electronic address: ordog.tamas@mayo.edu.
Mayo Clinic · USMayo Clinic in Florida · USWinnMed · US

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
UNDERGRADUATE RESEARCH AND TRAININGP20RR016464 · NCRR · UNIVERSITY OF NEVADA RENO · PI REIBER, CARL · 2001 to 2011
$30.3M
Physiological Characterization and Data Integration CoreP01DK068055 · NIDDK · MAYO CLINIC ROCHESTER · PI ORDOG, TAMAS · 2004 to 2019
$23.8M
PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI GREGORY J. GORES · 2009 to 2026
$22.2M
KLF10 regulates colitis through mediating TGFb induction of FOXP3 in Treg cells.R01AI089714 · NIAID · MAYO CLINIC ROCHESTER · PI FAUBION, WILLIAM A · 2011 to 2025
$6.3M
Interstitial Cells of Cajal in Diabetic GastropathyR01DK058185 · NIDDK · UNIVERSITY OF NEVADA RENO · PI ORDOG, TAMAS · 2002 to 2020
$5.2M
NCATS NIH HHS UL1 TR000135NCRR NIH HHS P20 RR016464NIAID NIH HHS R01 AI089714NIDDK NIH HHS P01 DK068055NIDDK NIH HHS P30 DK084567NIDDK NIH HHS R01 DK058185
6 · The paper itself

Abstract

BACKGROUND &

aimsAfter allogeneic transplantation, murine stem cells (SCs) for interstitial cells of Cajal (ICCs), electrical pacemaker, and neuromodulator cells of the gut, were incorporated into gastric ICC networks, indicating in vivo immunosuppression. Immunosuppression is characteristic of bone marrow- and other non-gut-derived mesenchymal stem cells (MSCs), which are emerging as potential therapeutic agents against autoimmune diseases, including inflammatory bowel disease. Therefore, we investigated whether gut-derived ICC-SCs could also mitigate experimental colitis and studied the mechanisms of ICC-SC-mediated immunosuppression in relation to MSC-induced pathways.

methodsIsolated ICC-SCs were studied by transcriptome profiling, cytokine assays, flow cytometry, mixed lymphocyte reaction, and T-cell proliferation assay. Mice with acute and chronic colitis induced by dextran sulfate sodium and T-cell transfer, respectively, were administered ICC-SCs intraperitoneally and evaluated for disease activity by clinical and pathological assessment and for ICC-SC homing by live imaging.

resultsUnlike strain-matched dermal fibroblasts, intraperitoneally administered ICC-SCs preferentially homed to the colon and reduced the severity of both acute and chronic colitis assessed by clinical and blind pathological scoring. ICC-SCs profoundly suppressed T-cell proliferation in vitro. Similar to MSCs, ICC-SCs strongly expressed cyclooxygenase 1/2 and basally secreted prostaglandin E2. Indomethacin, a cyclooxygenase inhibitor, countered the ICC-SC-mediated suppression of T-cell proliferation. In contrast, we found no role for regulatory T-cell-, programmed death receptor-, and transforming growth factor-β-mediated mechanisms reported in MSCs; and transcriptome profiling did not support a relationship between ICC-SCs and MSCs.

conclusionsMurine ICC-SCs belong to a class different from MSCs and potently mitigate experimental colitis via prostaglandin E2-mediated immunosuppression.

Indexed as

ColonImmunity, CellularStem Cell TransplantationAdoptive TransferAnimalsCell ProliferationCells, CulturedColitisDextran SulfateDinoprostoneDNA-Binding ProteinsGene Expression ProfilingGenetic MarkersHomeodomain ProteinsImmunocompromised HostInterstitial Cells of CajalDextran SulfateDinoprostoneDNA-Binding ProteinsGenetic MarkersHomeodomain ProteinsRAG-1 proteinRag2 protein, mouseIBDICCImmunosuppression

Identifiers

PMID25637652
PMCPMC4409492
OpenAlexW2099883038

What OpenQuestion holds

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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.