Evidence map›Paper›PMID 21047522›Full record

ArticleLife sciences2011

Role of anti-angiogenic factor endostatin in the pathogenesis of experimental ulcerative colitis.

Ganna Tolstanova, Xiaoming Deng, Tetyana Khomenko, Pallavi Garg, Brankica Paunovic, Longchuan Chen, Shanthi V Sitaraman, Joseph Shiloach, Sandor Szabo, Zsuzsanna Sandor

Open access · greenAbstract read
In one paragraph

Article in Life sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Stem Cell-Based Therapies for Inflammatory Bowel Disease.International journal of molecular sciences · 2022
    Review
  6. The Roles of Vascular Endothelial Growth Factor, Angiostatin, and Endostatin in Nasal Polyp Development.Journal of rhinology : official journal of the Korean Rhinologic Society · 2022
    Article
  7. Article
  8. Article
  9. Promoting inflammatory lymphangiogenesis by vascular endothelial growth factor-C (VEGF-C) aggravated intestinal inflammation in mice with experimental acute colitis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2016
    Article
  10. Angiogenesis in Inflammatory Bowel Disease.International journal of inflammation · 2015
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

10 authors at 3 institutions in 1 country.

Ganna TolstanovaDiagnostic & Molecular Medicine, Health Care Group, VA Medical Center, Long Beach, CA, USA.
Xiaoming Deng
Tetyana Khomenko
Pallavi Garg
Brankica Paunovic
Longchuan Chen
Shanthi V Sitaraman
Joseph Shiloach
Sandor Szabo
Zsuzsanna Sandor
University of California, Irvine · USEmory University · USCore Laboratories (United States) · US

Funding

Production and purification of biological compoundsZICDK015500 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SHILOACH, JOSEPH · 2009 to 2022
$7.2M
Intramural NIH HHS ZIC DK015500
6 · The paper itself

Abstract

aimsVascular endothelial growth factor (VEGF) and pathologic angiogenesis have been demonstrated to play a pathogenic role in the development and progression of inflammatory bowel disease. Thus, we hypothesized that the potent anti-angiogenic factor endostatin might play a beneficial role in experimental ulcerative colitis (UC). MAIN

methodsWe used three animal models of UC: (1) induced by 6% iodoacetamide (IA) in rats, or (2) by 3% dextran sulfate sodium (DSS) in matrix metalloproteinase-9 (MMP-9) knockout (KO) and wild-type mice, and (3) interleukin-10 (IL-10) KO mice. Groups of MMP-9 KO mice with DSS-induced UC were treated with endostatin or water for 5days. KEY

findingsWe found concomitant upregulation of VEGF, PDGF, MMP-9 and endostatin in both rat and mouse models of UC. A positive correlation between the levels of endostatin or VEGF and the sizes of colonic lesions was seen in IA-induced UC. The levels and activities of MMP-9 were also significantly increased during UC induced by IA and IL-10 KO. Deletion of MMP-9 decreased the levels of endostatin in both water- and DSS-treated MMP-9 KO mice. Treatment with endostatin significantly improved DSS-induced UC in MMP-9 KO mice. SIGNIFICANCE: 1) Concomitantly increased endostatin is a defensive response to the increased VEGF in UC, 2) MMP-9 is a key enzyme to generate endostatin which may modulate the balance between VEGF and endostatin during experimental UC, and 3) endostatin treatment plays a beneficial role in UC. Thus, anti-angiogenesis seems to be a new therapeutic option for UC.

Indexed as

AnimalsBlotting, WesternColitis, UlcerativeColonDextran SulfateDisease Models, AnimalEndostatinsEnzyme-Linked Immunosorbent AssayFemaleIodoacetamideMatrix Metalloproteinase 9MiceMice, KnockoutPlatelet-Derived Growth FactorRatsUp-RegulationDextran SulfateEndostatinsIodoacetamideMatrix Metalloproteinase 9Platelet-Derived Growth FactorVascular Endothelial Growth Factor A

Identifiers

PMID21047522
PMCPMC9552542
OpenAlexW2041608308

What OpenQuestion holds

Textmetadata
LicenceTDM
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.