Abstract
Abstract: :
Purpose: To investigate the role of lumican in the corneal wound healing response. Methods:Inflammatory responses of corneal epithelium debridement were compared in 2 months–old knock out mice lacking lumican (Lum–/–), keratocan (Kera–/–), and Kera–Lum/Lum–/– compound transgenic mice (overexpressing lumican driven by keratocan promoter in lumican knock out background). Wild type (Lum+/+) mice were used as control. A central 2 mm diameter epithelial debridement was created with Argerbrush® in corneas of anesthetized experimental mice. The injured corneas healed for 24 and 48 h were subjected to clinical and histological examinations. Results: The epithelium debridement of Lum–/– and Kera–/– mice healed slower than the wild type mice. Histological examination revealed that in wild type and Kera–/– mice, inflammatory cells (polynuclear neutrophils, PMN) appeared in stroma at the leading edge of the migrating epithelium at 12 hours after wounding and the number of PMN reached a peak in 24 hours. The PMN invasion was significantly retarded in the injured corneas of Lum–/– mice in comparison to wild type mice. Whereas in compound Kera–Lum/Lum–/– transgenic mice, infiltration of inflammatory cells was delayed and could be found at the central denuded cornea in 24 h at a time lumican was detected by immunohistochemistry. Conclusion: Lumican may serve as a regulatory protein in recruiting inflammatory cells into injured corneas.
Keywords: wound healing • cornea: epithelium • extracellular matrix