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Journal of the Korean Ophthalmological Society ; : 2378-2384, 1999.
Article in Korean | WPRIM | ID: wpr-28255

ABSTRACT

p53 suppressor gene expression and protein production increases in response to DNA damage and the subsequent cell cycle prolongation permits DNA repair or, in the severe cases, leads to apoptosis. These concepts led us to investigate the expression of p53 as a potential key regulator of DNA repair in the cornea after mechanical-and chemical-induced injury. Mechanical-induced injury was performed by denuding a4mmdiameter area of the central epithelium from the corneas of Sprague Dawley rats. Chemical-induced injury was performed by applying a 3.5 mmdiameter filter paper disc of saturated n-heptanol to the cornea. Samples were collected on the 1st 3rd and 7th day of treatment. We performed immunohistochemistry and Western blot analysis on corneal buttons. Control group did not receive any treatment. The immunohistochemical analysis demonstrated that p53 is localized in the anterior stromal keratocytes. Western blot analysis indicated p53 bandsin the lanes of the mechanically and the chemically injured corneas. Our results suggest that injury to the corneal epithelium triggers the activation of p53.


Subject(s)
Apoptosis , Blotting, Western , Cell Cycle , Cornea , DNA Damage , DNA Repair , Epithelium , Epithelium, Corneal , Genes, Suppressor , Heptanol , Immunohistochemistry , Rats, Sprague-Dawley
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