Evidence map›Paper›PMID 19478078›Full record

ArticleThe Journal of biological chemistry2009

S156C mutation in tissue inhibitor of metalloproteinases-3 induces increased angiogenesis.

Jian Hua Qi, Ganying Dai, Philip Luthert, Shyam Chaurasia, Joe Hollyfield, Bernhard H F Weber, Heidi Stöhr, Bela Anand-Apte

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.5field-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

29 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Drusen in patient-derived hiPSC-RPE models of macular dystrophies.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  17. Article
  18. Review
  19. Article
  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

8 authors at 4 institutions in 3 countries.

Jian Hua QiDepartment of Opthalmology, Cole Eye Institute, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, Cleveland, Ohio 44195, USA.
Ganying Dai
Philip Luthert
Shyam Chaurasia
Joe Hollyfield
Bernhard H F Weber
Heidi Stöhr
Bela Anand-Apte
University of Regensburg · DECase Western Reserve University · USCleveland Clinic Lerner College of Medicine · USInstitute of Ophthalmology · MX

Funding

Role of TIMP-3 in Ocular NeovascularizationR01EY016490 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI ANAND-APTE, BELA · 2005 to 2009
$1.7M
Inhibition of VEGF Mediated Angiogenesis by TIMP-3R01CA106415 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI ANAND-APTE, BELA · 2005 to 2009
$1.3M
Vision Research Infrastructure Development GrantR24EY015638 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI HOLLYFIELD, JOE GILBERT · 2004 to 2008
$1.1M
NCI NIH HHS CA106415NCI NIH HHS R01 CA106415NEI NIH HHS EY015638NEI NIH HHS EY016490NEI NIH HHS R01 EY016490NEI NIH HHS R24 EY015638
6 · The paper itself

Abstract

Tissue Inhibitor of metalloproteinases-3 (TIMP-3) is a potent matrix-bound angiogenesis inhibitor. Mutations in TIMP-3 cause Sorsby Fundus Dystrophy, a dominant inherited, early onset macular degenerative disease, with choroidal neovascularization causing a loss of vision in the majority of patients. Here we report that expression of S156C TIMP-3 mutation in endothelial cells results in an abnormal localization of the protein, increased glycosylation, decreased matrix metalloproteinase inhibitory activity, and increased vascular endothelial growth factor (VEGF) binding with a consequent increase in VEGF-dependent migration and tube formation. These enhanced signaling events appear to be mediated as a consequence of a post-transcriptionally regulated increase in the expression of membrane-associated VEGFR-2 in endothelial cells of Timp-3(156/156) mutant mice as well as in human Sorsby fundus dystrophy eyes. Understanding the mechanism(s) by which mutant TIMP-3 can induce abnormal neovascularization provides important insight into the pathophysiology of a number of diseases with increased angiogenesis.

Indexed as

ActinsAnimalsAortaCell MovementCell ProliferationCells, CulturedEndothelial CellsEyeGene ExpressionGlycosylationHumansMacular DegenerationMiceNeovascularization, PathologicPoint MutationProtein BindingActinsTIMP3 protein, humanTissue Inhibitor of Metalloproteinase-3Vascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID19478078
PMCPMC2740418
OpenAlexW2087020311

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.