Evidence map›Paper›PMID 25807183›Full record

ArticleMucosal immunology2015

The matricellular protein CCN1 promotes mucosal healing in murine colitis through IL-6.

J S Choi, K-H Kim, L F Lau

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.2field-weighted citation impact, top 8% 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, 68 citations in OpenAlex.

  1. Article
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  7. Article
  8. Role of Interleukin-6 Family Cytokines in Organ Fibrosis.Kidney diseases (Basel, Switzerland) · 2023
    Review
  9. Review
  10. Review
  11. Analysis of CCN Functions in Liver Regeneration After Partial Hepatectomy.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
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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

3 authors at 1 institution in 1 country.

J S ChoiDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois, USA.
K-H KimDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois, USA.
L F LauDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois, USA.
University of Illinois Chicago · US

Funding

Regulation of TNF-alpha by Integrin-Mediated Matrix SignalingR01GM078492 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAU, LESTER F · 2007 to 2018
$4.3M
The Matricellular Protein CCN1 in Wound HealingR01AR061791 · NIAMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAU, LESTER F · 2011 to 2021
$3.8M
Training--Signal Transduction and Cellular EndocrinologyT32DK007739 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ACKERMAN, STEVEN JULES · 1997 to 2011
$1.5M
NIAMS NIH HHS R01 AR061791NIAMS NIH HHS R01AR61791NIDDK NIH HHS T32 DK007739NIDDK NIH HHS T32 DK07739NIGMS NIH HHS R01 GM078492NIGMS NIH HHS R01GM78492
6 · The paper itself

Abstract

The matricellular protein CCN1 (CYR61) is known to function in wound healing and is upregulated in colons of patients with Crohn's disease and ulcerative colitis, yet its specific role in colitis is unknown. Here we have used Ccn1(dm/dm) knockin mice expressing a CCN1 mutant unable to bind integrins α6β1 and αMβ2 as a model to probe CCN1 function in dextran sodium sulfate (DSS)-induced colitis. Ccn1(dm/dm) mice exhibited high mortality, impaired mucosal healing, and diminished interleukin-6 (IL-6) expression during the repair phase of DSS-induced colitis compared with wild-type mice, despite having comparable severity of initial inflammation and tissue injury. CCN1-induced IL-6 expression in macrophages through integrin αMβ2 and in fibroblasts through α6β1, and IL-6 promoted intestinal epithelial cell (IEC) proliferation. Administration of purified CCN1 protein fully rescued Ccn1(dm/dm) mice from DSS-induced mortality, restored IEC proliferation and enhanced mucosal healing, whereas delivery of IL-6 partially rectified these defects. CCN1 therapy accelerated mucosal healing and recovery from DSS-induced colitis even in wild-type mice. These findings reveal a critical role for CCN1 in restoring mucosal homeostasis after intestinal injury in part through integrin-mediated induction of IL-6 expression, and suggest a therapeutic potential for activating the CCN1/IL-6 axis for treating inflammatory bowel disease.

Indexed as

AnimalsCell LineColitisCysteine-Rich Protein 61Disease Models, AnimalEnzyme-Linked Immunosorbent AssayFluorescent Antibody TechniqueHumansIn Situ Nick-End LabelingInterleukin-6Intestinal MucosaMiceMice, Inbred C57BLReverse Transcriptase Polymerase Chain ReactionWound HealingCCN1 protein, mouseCysteine-Rich Protein 61Interleukin-6

Identifiers

PMID25807183
PMCPMC4583322
OpenAlexW1997454502

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.