Establish an Cell Model to Explore the Impacts of UVA on Human Corneal Endothelial Wound Healing.

Purpose: To provide scientific data for clinical practice in making strategies for accelerating corneal endothelial wound healing, we investigated the impact of UVA on the corneal endothelial wound healing process and the underlying mechanism using an cell model.

Materials And Methods: An cell model for corneal endothelial wound healing was established by scratching the cultured human corneal endothelial cell (HCEnC) confluent layer. Then, we investigated the impacts of UVA irradiation and Ascorbic acid-2-phosphate (Asc-2p) on the wound healing process of the HCEnC model by examining wound-healing index, F-actin rate, Ki-67 rate, and ROS production.

Results: After scratching, the Ki-67 and F-actin HCEnCs occupied the scratching gap. Furthermore, the F-actin rates were significantly higher than Ki-67 rates in the wound closure area. After irradiated with UVA, the wound-healing indexes, Ki-67 rates and F-actin rates of the wound-healing model significantly reduced, whereas the ROS production significantly increased in a dose-dependent manner. Pretreatment with Asc-2p significantly reduced the ROS production as well as increased the wound-healing indexes, Ki-67rates and F-actin rates of the UVA irradiated wound-healing model.

Conclusion: The migration of HCEnC plays a major role in the wound healing process of the established cell model, which is like the wound healing process . UVA decreases the wound closure of the HCEnC model dose-dependently, while antioxidant Asc-2p can attenuate the damage to UVA to HCEnCs probably via reducing ROS to improve their migration.