title: Triamcinolone acetonide decreases outflow facility in C57BL/6 mouse eyes.
abstract: OBJECTIVE
  To determine the effect of triamcinolone acetonide (TA) on outflow facility in mice.
  
  
  METHODS
  Animals received 20 μL of TA (40 mg/mL) suspension subconjunctivally either bilaterally or unilaterally and were euthanized after either 1 week or 3 weeks. Before mice were killed, IOP was measured with a rebound tonometer. Outflow facility was determined using simultaneous pressure and flow measurements. Another set of animals received bilateral injection of anecortave acetate (AA) with or without bilateral TA injection and their outflow facility was also determined. Myocilin expression was investigated in a subset of eyes using quantitative PCR (qPCR).
  
  
  RESULTS
  Outflow facility of eyes in animals receiving bilateral TA injection (TA(BL)) and TA-treated eyes of animals receiving unilateral injection (TA(UL)) was significantly decreased compared to naïve control eyes (C(naive)) after 1 week and 3 weeks of TA treatment (ANOVA P < 0.01, P < 0.001, respectively). Eyes treated with AA (with or without TA) had higher outflow facility than animals treated with TA (P < 0.05). IOP data did not show any significant difference between groups. qPCR analysis revealed significant decrease in myocilin expression in eyes receiving AA compared to naïve control and TA-treated eyes (ANOVA P < 0.001).
  
  
  CONCLUSIONS
  Steroid treatment significantly decreases outflow facility in C57BL/6 mice despite having small effect on IOP. This animal model can be useful for studying the pathogenesis of steroid-induced glaucoma.
authors: Department of Cell Biology, SUNY Downstate Medical Center, Brooklyn, NY 11203, USA.
authors: Sandeep
authors: S
authors: Kumar
authors: Shaily
authors: S
authors: Shah
authors: Emily Rose
authors: ER
authors: Deutsch
authors: Hai Michael
authors: HM
authors: Tang
authors: John
authors: J
authors: Danias
mesh_terms: D000818:Animals; D003598:Cytoskeletal Proteins / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D005136:Eye Proteins / Q000235:genetics / Q000378:metabolism; D005260:Female; D005901:Glaucoma / Q000139:chemically induced* / Q000378:metabolism*; D005938:Glucocorticoids / Q000633:toxicity*; D006023:Glycoproteins / Q000235:genetics / Q000378:metabolism; D006854:Hydrocortisone / Q000031:analogs & derivatives / Q000633:toxicity; D007429:Intraocular Pressure / Q000187:drug effects / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D017551:Microdialysis / Q000379:methods; D008954:Models, Biological; D012333:RNA, Messenger / Q000378:metabolism; D014129:Trabecular Meshwork / Q000187:drug effects / Q000378:metabolism; D014222:Triamcinolone Acetonide / Q000633:toxicity*; D000099179:Myocilin
chemical_list: D003598:Cytoskeletal Proteins; D005136:Eye Proteins; D005938:Glucocorticoids; D006023:Glycoproteins; D006854:Hydrocortisone; D012333:RNA, Messenger; D014222:Triamcinolone Acetonide; D000099179:Myocilin; C108424:Anecortave