| First Author | Sumioka T | Year | 2014 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 55 |
| Issue | 5 | Pages | 3295-302 |
| PubMed ID | 24781945 | Mgi Jnum | J:229853 |
| Mgi Id | MGI:5754684 | Doi | 10.1167/iovs.13-13077 |
| Citation | Sumioka T, et al. (2014) Impairment of corneal epithelial wound healing in a TRPV1-deficient mouse. Invest Ophthalmol Vis Sci 55(5):3295-302 |
| abstractText | PURPOSE: To examine whether the absence or blockage of an ion channel receptor, transient receptor potential vanilloid subtype 1 (TRPV1), affects the healing of an epithelial injury using an experimental model of an epithelial defect in animal cornea. METHODS: The expression of TRPV1 in the corneal epithelium was examined using immunohistochemistry in mice and rats. The migration of the corneal epithelium was examined in epithelium-debrided rat cornea in organ culture in the presence or absence of a TRPV1 agonist or its antagonist. Epithelial migration and cell proliferation following the debridement were examined in the cornea of a TRPV1-null mouse. Real-time RT-PCR was performed in samples of healing corneas to analyze the expression pattern of epithelial migration-related components (i.e., IL-6, substance P, and TGF-beta1). RESULTS: TRPV1 was detected mainly in the basal layer of mouse or rat corneal epithelium. Adding a TRPV1 receptor agonist to the culture medium enhanced epithelial healing in the rat cornea, and a TRPV1 antagonist retarded it in organ culture. The loss of TRPV1 did not affect the histology of the mouse cornea. In vivo analysis showed the loss of TRPV1-impaired re-epithelialization of the debrided area of the corneal epithelium by the suppression of both cell migration and proliferation. The lack of TRPV1 suppressed the expression of IL-6 and substance P but not of TGF-beta1 in response to epithelial debridement in mice. CONCLUSIONS: TRPV1 signal is required for the upregulation of IL-6 and substance P and the healing of debrided corneal epithelium in mice. |
