Purpose: To study the expression levels of TRAIL and TRAIL receptor in the rat cornea after alkali burn. Methods: A 2mm2 filter paper embedded with a 0.5 M NaOH solution was applied in the centre of cornea for 30 sec, then we followed healing process up to 14 days. Immunostainings were done for TRAIL and TRAIL receptor. For western blot analysis, corneal epithelial cells from 5 different rats were pooled. Results: The immunostaining showed a strong up-regulation of TRAIL and TRAIL receptor in the nuclear and perinuclear area of corneal stroma and limbal cells. The intensity of the staining regained baseline levels few days later. After 14 days the central corneal stroma appeared to be as in the control eyes. In corneal epithelial cells, the chemical burn seems to not sensibly affect the expression of TRAIL. The chemical burn slightly upregulated the TRAIL receptor in corneal epithelial cells between 3 and 7 days following the healing of the tissues. In conjunctival cells alkali burn slightly raised up TRAIL from day 1 to 14. Instead, the expression of TRAIL receptor does not present a significant difference between treated and control eye. Conclusions: TRAIL may be a novel regulator and therapy target to treat chemically damaged cornea.
Increased TRAIL and TRAIL receptor expression in ratcorneal stroma exposed to chemical burn damage
Marialaura Amadio
2018-01-01
Abstract
Purpose: To study the expression levels of TRAIL and TRAIL receptor in the rat cornea after alkali burn. Methods: A 2mm2 filter paper embedded with a 0.5 M NaOH solution was applied in the centre of cornea for 30 sec, then we followed healing process up to 14 days. Immunostainings were done for TRAIL and TRAIL receptor. For western blot analysis, corneal epithelial cells from 5 different rats were pooled. Results: The immunostaining showed a strong up-regulation of TRAIL and TRAIL receptor in the nuclear and perinuclear area of corneal stroma and limbal cells. The intensity of the staining regained baseline levels few days later. After 14 days the central corneal stroma appeared to be as in the control eyes. In corneal epithelial cells, the chemical burn seems to not sensibly affect the expression of TRAIL. The chemical burn slightly upregulated the TRAIL receptor in corneal epithelial cells between 3 and 7 days following the healing of the tissues. In conjunctival cells alkali burn slightly raised up TRAIL from day 1 to 14. Instead, the expression of TRAIL receptor does not present a significant difference between treated and control eye. Conclusions: TRAIL may be a novel regulator and therapy target to treat chemically damaged cornea.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
