Evidence map›Paper›PMID 29928668›Full record

ArticleCellular and molecular gastroenterology and hepatology2018

Mesenteric Adipose-derived Stromal Cells From Crohn's Disease Patients Induce Protective Effects in Colonic Epithelial Cells and Mice With Colitis.

Jill M Hoffman, Aristea Sideri, Jonathan J Ruiz, Dimitris Stavrakis, David Q Shih, Jerrold R Turner, Charalabos Pothoulakis, Iordanes Karagiannides

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  5. Review
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  8. Review
  9. Adipose-derived Stromal Cells: The Good Side of Fat?Cellular and molecular gastroenterology and hepatology · 2018
    Article
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

8 authors at 3 institutions in 1 country.

Jill M HoffmanCenter for Inflammatory Bowel Diseases, Division of Digestive Diseases, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California.
Aristea SideriCenter for Inflammatory Bowel Diseases, Division of Digestive Diseases, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California.
Jonathan J RuizCenter for Inflammatory Bowel Diseases, Division of Digestive Diseases, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California.
Dimitris StavrakisCenter for Inflammatory Bowel Diseases, Division of Digestive Diseases, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California.
David Q ShihInflammatory Bowel and Immunobiology Research Institute, Cedars Sinai Medical Center, Los Angeles, California.
Jerrold R TurnerDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Charalabos PothoulakisCenter for Inflammatory Bowel Diseases, Division of Digestive Diseases, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California.
Iordanes KaragiannidesCenter for Inflammatory Bowel Diseases, Division of Digestive Diseases, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California.
University of California, Los Angeles · USBrigham and Women's Hospital · USCedars-Sinai Medical Center · US

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Women's Health and Functional Visceral Disorders CenterP50DK064539 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MAYER, EMERAN A · 2002 to 2017
$17.5M
ZO-1-MEDIATED PROTEIN INTERACTIONS: REGULATORS AND INTEGRATORS OF DIVERSE EPITHELIAL FUNCTIONS IN HEALTH AND DISEASER01DK061931 · NIDDK · UNIVERSITY OF CHICAGO · PI JERROLD R. TURNER · 2001 to 2026
$15.0M
Therapeutic targeting of protein interactions to reverse MLCK1-mediated intestinal barrier loss and ameliorate disease.R01DK068271 · NIDDK · UNIVERSITY OF CHICAGO · PI JERROLD R. TURNER · 2005 to 2026
$11.3M
SUBSTANCE P AND INTESTINAL INFLAMMATIONR01DK047343 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 1994 to 2014
$4.2M
Role of CRH receptor 2 in mucosal healing during colitisF32DK102322 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HOFFMAN, JILL MAY · 2014 to 2016
$169k
NIDDK NIH HHS F32 DK102322NIDDK NIH HHS P30 DK041301NIDDK NIH HHS P50 DK064539NIDDK NIH HHS R01 DK047343NIDDK NIH HHS R01 DK068271
6 · The paper itself

Abstract

Mesenteric adipose tissue hyperplasia is a hallmark of Crohn's disease (CD). Recently, we showed that mesenteric adipose-derived stromal cells (ADSCs) from CD, ulcerative colitis, and control patients synthesize and release adipokines in a disease-dependent manner. Here we examined the expression profiles of CD and control patient-derived mesenteric ADSCs and studied the effects of their extracellular mediators on colonocyte signaling in vitro and experimental colitis in vivo. ADSCs were isolated from mesenteric fat of control and CD patients. Microarray profiling and network analysis were performed in ADSCs and human colonocytes treated with conditioned media from cultured ADSCs. Mice with acute colitis received daily injections of conditioned media from patient-derived ADSCs, vehicle, or apolactoferrin. Proliferative responses were evaluated in conditioned media-treated colonocytes and mouse colonic epithelium. Total protein was isolated from cultured colonocytes after treatment with apolactoferrin for Western blot analysis of phosphorylated intracellular signaling kinases. Microarray profiling revealed differential mRNA expression in CD patient-derived ADSCs compared with controls, including lactoferrin. Administration of CD patient-derived medium or apolactoferrin increased colonocyte proliferation compared with controls. Conditioned media from CD patient-derived ADSCs or apolactoferrin attenuated colitis severity in mice and enhanced colonocyte proliferation in vivo. ADSCs from control and CD patients show disease-dependent inflammatory responses and alter colonic epithelial cell signaling in vitro and in vivo. Furthermore, we demonstrate lactoferrin production by adipose tissue, specifically mesenteric ADSCs. We suggest that mesenteric ADSC-derived lactoferrin may mediate protective effects and participate in the pathophysiology of CD by promoting colonocyte proliferation and the resolution of inflammation.

Indexed as

ADSC, adipose-derived stromal cellCD, Crohn’s diseaseDSS, dextran sodium sulfateIBD, inflammatory bowel diseaseIBS, irritable bowel syndromei.c., intracolonicIL, interleukinInflammatory Bowel DiseaseIntestinal EpitheliumMesenteric Adipose TissuePCR, polymerase chain reactionPreadipocytesRT, reverse-transcriptaseTNBS, trinitrobenzenesulfonic acidVEGF, vascular endothelial growth factor

Identifiers

PMID29928668
PMCPMC6008259
OpenAlexW2794106515

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.