Open AccessImpact of triamcinolone acetonide on retinal endothelial cells in a retinopathy of prematurity mouse model
Author(s) -
Akkoyun Imren,
Yilmaz Gursel,
Oto Sibel,
Kahraman Burcu,
Haberal Nihan,
Akova Yonca A.
Publication year - 2007
Publication title -
acta ophthalmologica scandinavica
Language(s) - English
Resource type - Journals
eISSN - 1600-0420
pISSN - 1395-3907
DOI - 10.1111/j.1600-0420.2007.00945.x
Subject(s) - triamcinolone acetonide , retinopathy of prematurity , medicine , retinal , neovascularization , endothelial stem cell , in vivo , ophthalmology , retina , acetonide , andrology , angiogenesis , in vitro , biology , biochemistry , gestational age , pregnancy , genetics , microbiology and biotechnology , neuroscience
. Purpose: To evaluate the efficacy of different concentrations of triamcinolone acetonide (TA) on retinal endothelial cell proliferation in a retinopathy of prematurity (ROP) mouse model. Methods: A total of 24 C57BL/J6 mice were exposed to 75% oxygen from postnatal day 7 to day 12. On day 12, 10 mice (group B) were injected with 20 µg intravitreal TA (IVTA) and 14 mice (group C) were injected with 40 µg IVTA in one eye. The contralateral eyes were injected with isotonic saline (control group = group A). Four non‐exposed mice served as negative controls (group D). The mice were killed on day 17 and the eyes removed for quantitative analysis of preretinal neovascularization. Neovascularization was quantified by counting the endothelial cell nuclei on the vitreal side of the inner limiting membrane of the retina. Results: The endothelial cell count per histological section was lower in groups B (1.4 ± 1.7 cells; p < 0.00001) and C (0.9 ± 1.4 cells; p < 0.1) compared with the control group (group A, 17.0 ± 4.8 cells). However, there was no significant difference in cell count between groups B and C (p = 0.430). Conclusions: Triamcinolone acetonide suppresses endothelial cell proliferation in an ROP mouse model in vivo . There is no difference between dosages of 20 µg and 40 µg IVTA in experimental use in the suppression rates of endothelial cell proliferation.