Abstract
Purpose :
A mouse model by coagulating the first branch of the trigeminal nerve delays corneal epithelial wound healing and simultaneously decreases expression of the perception-related cation channels TRPV4 and TRPA1 mRNA in the peripheral cornea (Lab invest, 2019). In this study, we investigated the effect of forced TRPA1 gene expression in this model.
Methods :
Using previously reported methods, a model of neurotrophic keratopathy was created coagulating the first branch of the trigeminal nerve by 20-gauge bipolar needle. In this model, corneal epithelial wound healing is delayed, although corneal transparency is maintained.
(1) Three months after trigeminal coagulation, TRPA1 adeno-associated virus vector (TRPA1-AAV) (n=6) or control-AAV (n=6) was injected into the coagulated nerve. Four weeks after injection, epithelial defect (2mm diameter) were created in the cornea, and the rate of wound closure was compared by photographing the defects every 6 hours.
(2) The proliferation activity of the healing epithelium was determined by uisng BrdU-labeling in both group mice after 12 or 24hrs.
Results :
(1) TRPA1-AAV group showed significantly smaller epithelial defects in the healing process after 6 and 12 hrs compared with control-AAV group. (2) BrdU-positive cells were increased after 12 and 24 hrs by TRA1-AAV group as compared with control AAV group in central and peripheral corneal epithelium.
Conclusions :
Expression of TRPA1 in the injured trigeminal nerve restored the delayed corneal epithelial wound healing associated with neurotrophic keratopathy. TRPA1 channels are potential therapeutic targets for neurotrophic keratopathy.
This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.