Evidence map›Paper›PMID 25114380›Full record

ArticleMediators of inflammation2014

Impaired resolution of inflammation in the Endoglin heterozygous mouse model of chronic colitis.

Madonna R Peter, Mirjana Jerkic, Valentin Sotov, David N Douda, Daniela S Ardelean, Niousha Ghamami, Flavia Lakschevitz, Meraj A Khan, Susan J Robertson, Michael Glogauer and 3 more

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

Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Trial
  2. Article
  3. Targeting Angiogenesis via Resolution of Inflammation.Cold Spring Harbor perspectives in medicine · 2023
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

13 authors at 3 institutions in 1 country.

Madonna R PeterMolecular Structure and Function Program, The Hospital for Sick Children, Toronto, ON, Canada M5G 0A4 ; Department of Immunology, University of Toronto, Toronto, ON, Canada M5S 1A8.
Mirjana JerkicMolecular Structure and Function Program, The Hospital for Sick Children, Toronto, ON, Canada M5G 0A4 ; Keenan Research Centre in Li Ka Shing Knowledge Institute, St. Michael's Hospital, 209 Victoria Street, Toronto, ON, Canada M5B 1T8.ORCID 0000-0002-0623-0347
Valentin SotovMolecular Structure and Function Program, The Hospital for Sick Children, Toronto, ON, Canada M5G 0A4 ; Department of Immunology, University of Toronto, Toronto, ON, Canada M5S 1A8.
David N DoudaProgram in Physiology and Experimental Medicine, The Hospital for Sick Children, Toronto, ON, Canada M5G 0A4 ; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada M5S 1A8.
Daniela S ArdeleanMolecular Structure and Function Program, The Hospital for Sick Children, Toronto, ON, Canada M5G 0A4 ; Department of Immunology, University of Toronto, Toronto, ON, Canada M5S 1A8 ; Division of Rheumatology, Department of Pediatrics, The Hospital for Sick Children, Toronto, ON, Canada M5G 1X8.
Niousha GhamamiMolecular Structure and Function Program, The Hospital for Sick Children, Toronto, ON, Canada M5G 0A4.ORCID 0000-0003-0063-7629
Flavia LakschevitzDepartment of Periodontology, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada M5G 1G6.ORCID 0000-0001-6693-1906
Meraj A KhanProgram in Physiology and Experimental Medicine, The Hospital for Sick Children, Toronto, ON, Canada M5G 0A4.
Susan J RobertsonDepartment of Immunology, University of Toronto, Toronto, ON, Canada M5S 1A8.
Michael GlogauerDepartment of Periodontology, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada M5G 1G6.ORCID 0000-0002-6248-5977
Dana J PhilpottDepartment of Immunology, University of Toronto, Toronto, ON, Canada M5S 1A8.
Nades PalaniyarProgram in Physiology and Experimental Medicine, The Hospital for Sick Children, Toronto, ON, Canada M5G 0A4 ; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada M5S 1A8 ; Institute of Medical Science, University of Toronto, Toronto, ON, Canada M5S 1A8.ORCID 0000-0002-2170-8548
Michelle LetarteMolecular Structure and Function Program, The Hospital for Sick Children, Toronto, ON, Canada M5G 0A4 ; Department of Immunology, University of Toronto, Toronto, ON, Canada M5S 1A8.ORCID 0000-0002-5901-7582
University of Toronto · CAHospital for Sick Children · CASt. Michael's Hospital · CA

Funding

Canadian Institutes of Health Research MOP-111012Canadian Institutes of Health Research MOP-6247
6 · The paper itself

Abstract

Endoglin is a coreceptor of the TGF-β superfamily predominantly expressed on the vascular endothelium and selective subsets of immune cells. We previously demonstrated that Endoglin heterozygous (Eng (+/-)) mice subjected to dextran sulfate sodium (DSS) developed persistent gut inflammation and pathological angiogenesis. We now report that colitic Eng (+/-) mice have low colonic levels of active TGF-β1, which was associated with reduced expression of thrombospondin-1, an angiostatic factor known to activate TGF-β1. We also demonstrate dysregulated expression of BMPER and follistatin, which are extracellular regulators of the TGF-β superfamily that modulate angiogenesis and inflammation. Heightened colonic levels of the neutrophil chemoattractant and proangiogenic factor, CXCL1, were also observed in DSS-treated Eng (+/-) mice. Interestingly, despite increased macrophage and neutrophil infiltration, a gut-specific reduction in expression of the key phagocytic respiratory burst enzymes, NADPH oxidase 2 (Nox-2) and myeloperoxidase, was seen in Eng (+/-) mice undergoing persistent inflammation. Taken together, these findings suggest that endoglin is required for TGF-β superfamily mediated resolution of inflammation and fully functional myeloid cells.

Indexed as

AnimalsChemokine CXCL1ColitisDisease Models, AnimalEndoglinHeterozygoteInflammationIntracellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLSignal TransductionTransforming Growth Factor beta1Chemokine CXCL1EndoglinEng protein, mouseIntracellular Signaling Peptides and ProteinsTransforming Growth Factor beta1

Identifiers

PMID25114380
PMCPMC4121192
OpenAlexW2107144435

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.