Document Detail


Chemical Injury-Induced Corneal Opacity and Neovascularization Reduced by Rapamycin via TGF- β1/ERK Pathways Regulation.
MedLine Citation:
PMID:  23716625     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
PURPOSE: To investigate the protective effect of rapamycin against alkali burn-induced corneal damage in mice. METHODS: BALB/c mice were treated with 0.1 N sodium hydroxide (NaOH) onto the cornea for 30 s. Corneal neovascularization and opacity were clinically evaluated at 1 week, 2 weeks, and 4 weeks after chemical burn injury. Rapamycin (Sigma, St. Louis, MO) was delivered into right eyes topically (1 mg/mL) and intraperitoneally injected (0.2 mg/kg) once a day. The concentrations of interleukin-6 (IL-6) and transforming growth factor-beta1 (TGF-β1) in the cornea were measured by ELISA. In vitro cultured human corneal stromal cells were treated with 0 - 500 nM rapamycin for 3 days and then assessed by immunofluorescence staining of vimentin and alpha-smooth muscle actin (α-SMA). Western blotting for α-SMA, phosphorylated extracellular signal-regulated kinase (ρ-ERK 1/2), and total ERK 1/2 was also performed. RESULTS: Corneal-neovascularization and corneal-opacity scores, measured 4 weeks after the chemical burn corneal injury, were lower in the rapamycin group than in the control group. Two weeks after the chemical burn injury, a significant elevation in the corneal IL-6 levels of the positive control group was observed, as compared to the levels in the negative control group or the rapamycin group (p < 0.05). Corneal TGF-β1 levels were lower in the rapamycin-treated group than in the control group at 4 weeks after chemical burn injury (p < 0.05). Moreover, rapamycin inhibited TGF-β1-induced α-SMA expression and augmented ERK 1/2 phosphorylation. CONCLUSIONS: Rapamycin treatment reduced corneal opacity and corneal neovascularization in BALB/c mice. Rapamycin protected the cornea from chemical damage via reduction of IL-6 and TGF-β1 expression. Rapamycin reduced alpha-SMA expression through ERK 1/2 pathway.
Authors:
Young Joo Shin; Joon Young Hyon; Won Seok Choi; Kayoung Yi; Eui-Sang Chung; Tae-Young Chung; Won Ryang Wee
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-5-28
Journal Detail:
Title:  Investigative ophthalmology & visual science     Volume:  -     ISSN:  1552-5783     ISO Abbreviation:  Invest. Ophthalmol. Vis. Sci.     Publication Date:  2013 May 
Date Detail:
Created Date:  2013-5-30     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7703701     Medline TA:  Invest Ophthalmol Vis Sci     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Department of Ophthalmology, Hallym University College of Medicine, 948-1 Daerim1-dong, Youngdeungpo-gu, Seoul, 150-950, Korea (South), Republic of.
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