Evidence map›Paper›PMID 18599605›Full record

ArticleThe American journal of pathology2008

Substance P-mediated expression of the pro-angiogenic factor CCN1 modulates the course of colitis.

Hon-Wai Koon, Dezheng Zhao, Hua Xu, Collin Bowe, Alan Moss, Mary P Moyer, Charalabos Pothoulakis

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. MiR-21 in Substance P-induced exosomes promotes cell proliferation and migration in human colonic epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2019
    Article
  5. Article
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  8. Review
  9. Article
  10. Article
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  12. Article
  13. Novel roles of perivascular nerves on neovascularization.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2015
    Review
  14. Article
  15. Article
  16. Role of cysteine-rich 61 protein (CCN1) in macrophage-mediated oncolytic herpes simplex virus clearance.Molecular therapy : the journal of the American Society of Gene Therapy · 2014
    Article
  17. Review
  18. Review
  19. Article
  20. CCN1/CYR61: the very model of a modern matricellular protein.Cellular and molecular life sciences : CMLS · 2011
    Review
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 3 institutions in 1 country.

Hon-Wai KoonGastrointestinal Neuropeptide Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Dezheng Zhao
Hua Xu
Collin Bowe
Alan Moss
Mary P Moyer
Charalabos Pothoulakis
Beth Israel Deaconess Medical Center · USUniversity of California, Los Angeles · USIncell Corporation (United States) · US

Funding

SUBSTANCE P AND INTESTINAL INFLAMMATIONR01DK047343 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 1994 to 2014
$4.2M
NIDDK NIH HHS DK 47343NIDDK NIH HHS R01 DK047343
6 · The paper itself

Abstract

Substance P (SP) regulates important intestinal functions, such as mucosal permeability, motility, chloride secretion, and inflammation via the neurokinin-1 receptor (NK-1R). Previous reports showed that vascularization and expression of angiogenic factors are evident in the colonic mucosa of rats with colitis and patients with inflammatory bowel disease. Here we determined whether SP is associated with angiogenesis. Human NCM460 colonocytes stably transfected with the human NK-1R (NCM460-NK-1R cells) and mice with dextran sodium sulfate-induced colitis were used. We found that expression of the angiogenic factor CCN1 was increased in the colons of patients with Crohn's disease and ulcerative colitis. Mucosal extracts from inflammatory bowel disease patients induced human intestinal microvascular endothelial cell migration that was inhibited by blockade of CCN1 and its receptor integrin alphavbeta3. Both the degree of angiogenesis and CCN1 expression were elevated in the colons of mice with dextran sodium sulfate-induced colitis, which was reduced by treatment with the NK-1R antagonist CJ-12255. SP also increased CCN1 expression in NCM460-NK-1R colonocytes. SP exposure to human intestinal microvascular endothelial cells co-cultured with NCM460-NK-1R cells induced angiogenic activity that was inhibited by CCN1 silencing. In addition, intracolonic overexpression of CCN1 induced angiogenesis in mouse colon. Thus, SP mediates angiogenesis via CCN1 during colitis.

Indexed as

AnimalsBridged Bicyclo Compounds, HeterocyclicCell MovementColitis, UlcerativeColonCrohn DiseaseCysteine-Rich Protein 61Dextran SulfateEndothelial CellsEndothelium, VascularHumansImmediate-Early ProteinsIntegrin alphaVbeta3Intercellular Signaling Peptides and ProteinsMaleMice6-diphenylmethyl-5-(5-isopropyl-2-methoxybenzylamino)-1-azabicyclo(2.2.2)octane-3-carboxylic acidBridged Bicyclo Compounds, HeterocyclicCCN1 protein, humanCCN1 protein, mouseCysteine-Rich Protein 61Dextran SulfateImmediate-Early ProteinsIntegrin alphaVbeta3Intercellular Signaling Peptides and ProteinsReceptors, Neurokinin-1Substance P

Identifiers

PMID18599605
PMCPMC2475777
OpenAlexW2078535342

What OpenQuestion holds

Textmetadata
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.