title: Treatment with triamcinolone acetonide prevents decreased retinal levels of decorin in a rat model of oxygen-induced retinopathy.
abstract: OBJECTIVE
  To investigate the effect of triamcinolone acetonide (TA) on retinal expression of decorin in a rat model of oxygen-induced retinopathy (OIR).
  
  
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Ophthalmology, School of Medicine, Institute of Health Science, Gyeongsang National University, Jinju, Gyeongnam, Korea, Republic of Korea.
authors.forename: Yeon-Jeong
authors.initials: YJ
authors.lastname: Park
authors.forename: Young-Hee
authors.initials: YH
authors.lastname: Kim
authors.forename: Wan-Sung
authors.initials: WS
authors.lastname: Choi
authors.forename: In-Young
authors.initials: IY
authors.lastname: Chung
authors.forename: Ji-Myong
authors.initials: JM
authors.lastname: Yoo
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D015153:Blotting, Western; D016923:Cell Death; D058575:Decorin; D004195:Disease Models, Animal; D016326:Extracellular Matrix Proteins / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D018496:Hyperoxia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D007231:Infant, Newborn; D010100:Oxygen / Q000633:toxicity; D011247:Pregnancy; D011509:Proteoglycans / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000378:metabolism*; D012165:Retinal Ganglion Cells / Q000187:drug effects / Q000473:pathology; D012178:Retinopathy of Prematurity / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014222:Triamcinolone Acetonide / Q000627:therapeutic use*
chemical_list: C546878:DCN protein, human; C546880:Dcn protein, rat; D058575:Decorin; D016326:Extracellular Matrix Proteins; D005938:Glucocorticoids; D011509:Proteoglycans; D012333:RNA, Messenger; D014222:Triamcinolone Acetonide; D010100:Oxygen