| Presentation preference | Invited lecture |
| Title | Role of TRP channels for neurotrophic keratopathy |
| Accept poster if oral is not possible ? | No |
| Purpose | To understand pathobiology of neurotrophic keratopathy we established a mouse model of neurotrophic keratopathy by coagulating the first branch of the trigeminal nerve (V1 nerve). Impaired corneal epithelial healing in the model mouse was associated with suppression of both cell proliferation and expression of stem cell markers in peripheral/limbal epithelium as well as reduction of transient receptor potential (TRP) channel expression in tissue. |
| Methods | Six to 8 week-old male C57BL/6 mice underwent stereotactic trigeminal coagulation to destroy the ophthalmic branch (V1) of right trigeminal nerve as previously reported (Okada et al. Lab invest, 2018). In this model corneal epithelium did not breakdown without external insult, but showed impaired epithelial healing after producing a defect. |
| Results | TRPV4 and TRPA1gene introduction into a damaged V1 nerve rescues the impairment of epithelial healing in association with partial recovery of the stem/progenitor cell markers and upregulation of cell proliferation. |
| Conclusion | The role of TRP channels in the therapeutic effect of TRPV4 and TRPA1 AAV on neurotrophic keratopathy on corneal scarring and inflammation are important. |
| Conflict of interest | No |
1
| Last name | OKADA |
| Initials of first name(s) | Y |
| Department | Ophthalmology, Wakayama Medical University, Kihoku Hospital |
| City | Katuragi |
| Country | Japan |