Evidence map›Paper›PMID 20398651›Full record

ArticleExperimental eye research2010

Genetic deletion of COX-2 diminishes VEGF production in mouse retinal Müller cells.

Susan E Yanni, Gary W McCollum, John S Penn

Abstract read
In one paragraph

Article in Experimental eye research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Lipid Signaling in Ocular Neovascularization.International journal of molecular sciences · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Viral Retinopathy in Experimental Models of Zika Infection.Investigative ophthalmology & visual science · 2017
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Celecoxib attenuates retinal angiogenesis in a mouse model of oxygen-induced retinopathy.International journal of clinical and experimental pathology · 2015
    Article
  20. Mitigation of oxygen-induced retinopathy in α2β1 integrin-deficient mice.Investigative ophthalmology & visual science · 2014
    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

3 authors at 1 institution in 1 country.

Susan E YanniDepartment of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232-8808, USA. Susan.e.yanni@gmail.com
Gary W McCollum
John S Penn
Vanderbilt University · US

Funding

RETINOPATHY OF PREMATURITY--UNDERSTAND ITS PATHOGENESISR01EY007533 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PENN, JOHN S. · 1993 to 2018
$7.0M
ANIMAL MODEL FOR RETINOPATHY OF PREMATURITYR29EY007533 · NEI · UNIVERSITY OF ARKANSAS MED SCIS LTL ROCK · PI PENN, JOHN S. · 1988 to 1992
–
NEI NIH HHS EY01826NEI NIH HHS EY07533NEI NIH HHS R01 EY007533
6 · The paper itself

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs), which inhibit COX activity, reduce the production of retinal VEGF and neovascularization in relevant models of ocular disease. We hypothesized that COX-2 mediates VEGF production in retinal Müller cells, one of its primary sources in retinal neovascular disease. The purpose of this study was to determine the role of COX-2 and its products in VEGF expression and secretion. These studies have more clearly defined the role of COX-2 and COX-2-derived prostanoids in retinal angiogenesis. Müller cells derived from wild-type and COX-2 null mice were exposed to hypoxia for 0-24 h. COX-2 protein and activity were assessed by western blot analysis and GC-MS, respectively. VEGF production was assessed by ELISA. Wild-type mouse Müller cells were treated with vehicle (0.1% DMSO), 10 microM PGE(2), or PGE(2) + 5 microM H-89 (a PKA inhibitor), for 12 h. VEGF production was assessed by ELISA. Hypoxia significantly increased COX-2 protein (p < 0.05) and activity (p < 0.05), and VEGF production (p < 0.0003). COX-2 null Müller cells produced significantly less VEGF in response to hypoxia (p < 0.05). Of the prostanoids, PGE(2) was significantly increased by hypoxia (p < 0.02). Exogenous PGE(2) significantly increased VEGF production by Müller cells (p < 0.0039), and this effect was inhibited by H-89 (p < 0.055). These data demonstrate that hypoxia induces COX-2, prostanoid production, and VEGF synthesis in Müller cells, and that VEGF production is at least partially COX-2-dependent. Our study suggests that PGE(2), signaling through the EP(2) and/or EP(4) receptor and PKA, mediates the VEGF response of Müller cells.

Indexed as

AnimalsAnimals, NewbornBlotting, WesternCells, CulturedCyclic AMP-Dependent Protein KinasesCyclooxygenase 2DinoprostoneEnzyme-Linked Immunosorbent AssayGas Chromatography-Mass SpectrometryGene DeletionHypoxiaIsoquinolinesMiceMice, Inbred C57BLMice, KnockoutMicrogliaCyclic AMP-Dependent Protein KinasesCyclooxygenase 2DinoprostoneIsoquinolinesN-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamideProstaglandinsProtein Kinase InhibitorsPtgs2 protein, mouseSulfonamidesVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID20398651
PMCPMC2879458
OpenAlexW2062576746

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.