Evidence map›Paper›PMID 17065516›Full record

ArticleInvestigative ophthalmology & visual science2006

Triamcinolone reduces neovascularization, capillary density and IGF-1 receptor phosphorylation in a model of oxygen-induced retinopathy.

M Elizabeth Hartnett, David J Martiniuk, Yuta Saito, Pete Geisen, Lynda J Peterson, Janet R McColm

Open access · hybridAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.1field-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

16 citing papers in PubMed, 30 citations in OpenAlex.

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  13. Effect of intravitreal triamcinolone acetonide on retinal apoptosis in experimental retinal neovascularization.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2008
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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

6 authors at 1 institution in 1 country.

M Elizabeth HartnettDepartment of Ophthalmology, University of North Carolina, 6109A Neuroscience Research Building, Chapel Hill, NC 27599, USA. hartnet@med.unc.edu
David J Martiniuk
Yuta Saito
Pete Geisen
Lynda J Peterson
Janet R McColm
University of North Carolina at Chapel Hill · US

Funding

Mechanisms of Angiogenesis of Retinopathy of PrematurityR01EY015130 · NEI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Mary Elizabeth Ruth Hartnett · 2005 to 2026
$7.6M
NEI NIH HHS R01 EY 015130NEI NIH HHS R01 EY015130
6 · The paper itself

Abstract

purposeTo study the effects of intravitreous triamcinolone acetonide (TA) on neovascularization (NV), capillary density, and retinal endothelial cell (REC) viability in a model of oxygen-induced retinopathy (OIR).

methodsNewborn rats exposed to OIR underwent intravitreous injections (right eye) at day 14 to achieve intravitreous concentrations of: dexamethasone (DEX) (0.3 mg/mL), triamcinolone (TA; 0.4-4 mg/mL), or PBS. Animals were removed to room air and at day 18, retinal flatmounts were assayed for clock hours of NV, percent peripheral avascular retina, capillary density, apoptosis, and VEGF protein. At day 15, retinas were assayed for insulin-like growth factor (IGF)-1 receptor phosphorylation (IGF-1Rphos). Human RECs exposed to TA were assayed for trypan blue exclusion or activated caspase-3.

resultsTA but not DEX or PBS reduced NV (ANOVA, P < 0.001), capillary density (ANOVA, P < 0.001), and systemic weight gain (ANOVA, P = 0.002). VEGF protein was not different between TA- and PBS-injected or noninjected groups. Apoptosis was not increased in vivo or in vitro between groups, but there was a dose-dependent toxic effect of TA on cultured RECs (P < 0.001). At day 15, retinas from the 4 mg/mL TA-injected OIR group had a trend toward reduced IGF-1Rphos compared with room air-raised PBS- or non-injected OIR groups.

conclusionsTA caused dose-dependent reductions in NV, retinal vascularization, and systemic weight gain associated with a reduction in IGF-1Rphos. Long-term studies are needed to assess TA toxicity in vivo. TA doses should be carefully considered before administering the drug in diseases with ongoing retinal vascular development, such as retinopathy of prematurity.

Indexed as

Disease Models, AnimalAnimalsAnimals, NewbornApoptosisCapillariesDexamethasoneDose-Response Relationship, DrugEndothelium, VascularGlucocorticoidsHumansInfant, NewbornInjectionsOxygenPhosphorylationRatsRats, Sprague-DawleyDexamethasoneGlucocorticoidsOxygenReceptor, IGF Type 1Triamcinolone AcetonideVascular Endothelial Growth Factor Avascular endothelial growth factor A, rat

Identifiers

PMID17065516
PMCPMC1828044
OpenAlexW2067860427

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.