Treatment With Triamcinolone Acetonide Prevents Decreased Retinal Levels of Decorin in a Rat Model of Oxygen-Induced Retinopathy

• Published in: Current eye research Vol. 35; no. 7; pp. 657 - 663
• Main Authors: Park, Yeon-Jeong, Kim, Young-Hee, Choi, Wan-Sung, Chung, In-Young, Yoo, Ji-Myong
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 01.07.2010; Taylor & Francis
• Subjects: Animals; Animals, Newborn; Blotting, Western; Cell Death; Decorin; Disease Models, Animal; Extracellular Matrix Proteins - genetics; Extracellular Matrix Proteins - metabolism; Female; Ganglion cells; Glucocorticoids - therapeutic use; Humans; Hyperoxia - drug therapy; Hyperoxia - metabolism; Hyperoxia - pathology; Immunohistochemistry; In Situ Nick-End Labeling; Infant, Newborn; Oxygen - toxicity; Oxygen-induced retinopathy; Pregnancy; Proteoglycans - genetics; Proteoglycans - metabolism; Rats; Rats, Sprague-Dawley; Retina - metabolism; Retinal Ganglion Cells - drug effects; Retinal Ganglion Cells - pathology; Retinal neurons; Retinopathy of Prematurity - drug therapy; Retinopathy of Prematurity - metabolism; Retinopathy of Prematurity - pathology; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - metabolism; Triamcinolone acetonide; Triamcinolone Acetonide - therapeutic use
• ISSN: 0271-3683; 1460-2202
• DOI: 10.3109/02713681003760143

Purpose: To investigate the effect of triamcinolone acetonide (TA) on retinal expression of decorin in a rat model of oxygen-induced retinopathy (OIR). Materials and Methods: OIR was stimulated by exposing Sprague-Dawley (SD) rats to hyperoxia (80 ± 1.3% O2) from postnatal day (P) 2 to P14 and then returning them to normoxia (room air, 21 ± 1.5% O2). Control rats were maintained in normoxia. At P15, TA (40 mg/ml) was injected into the right vitreous of OIR rats and saline into the left vitreous of control rats. All rats were sacrificed at P18. RT-PCR, western blot and immunohistochemistry, TUNEL assay were performed to detect the effects of TA on molecular and morphological changes in retinal decorin levels in P18 OIR rats. Results: In P18 OIR rats, mRNA and protein of retinal levels and immunoreactivity of retinal decorin were significantly less (p-value = 0.0000000012, 0.0007, 0.000003; n = 5; respectively) than in control rats. In addition, neuronal cell death was increased in P18 OIR rats (p-value = 0.0028; n = 5) relative to controls. However, treatment with TA prevented the decrease of mRNA, protein levels, and immunoreactivity in retinal decorin in P18 OIR rats (p-value = 0.00023, 0.003, 0.000079; n = 5, respectively), and restored neuronal cell death in P18 OIR rats (p-value = 0.0022, n = 5). Conclusion: Our results suggest that decorin is involved in hypoxic retinal damage and that TA protects retinal neurons damaged by relative hypoxia from decreased decorin levels.