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Yuka Okada, Kumi Shirai, Peter S Reinach, Masayasu Miyajima, Shizuya Saika; Impairment of cornea epithelium wound healing in a TRPA1-deficient mouse. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):703.
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© ARVO (1962-2015); The Authors (2016-present)
To examine if gene ablation of transient receptor potential ankyrin 1 (TRPA1), a cation channel receptor, affects healing of an experimental epithelial defect in a mouse cornea. TRPA1 is co-expressed with TRPV1 in corneal sensory nerve fibers and basal epithelial cells. We previously reported that gene knockout of TRPV1, another TRP family member, retarded epithelial healing in mice.
Healing of debridement of central corneal epithelium was examined in C57BL/6 (wild type, WT, n = 16) and TRPV1-null (KO, n = 16) mice. A round epithelial debridement (2.0 mm in diameter) was produced in the central cornea of the right eye in KO and WT mice. At healing intervals up to 36 hrs the remaining defect of the epithelium was determined by using green fluorescein staining. In another series of experiment the proliferation activity of the healing epithelium was determined by uisng BrdU-labeling in WT and KO mice. Real-time RT-PCR was performed in samples of the healing corneas to analyze the expression pattern of epithelial migration-related components, i. e., interleukin 6 (IL-6), substance P and transforming growth factor b1 (TGFb1).
At 18 to 24 hrs post-debridement the defect remaining was larger in KO mice as compared with WT mice. BrdU-labeled cells were less frequently observed in KO healing epithelium as compared with WT cornea at 24 and 36 hrs post-wounding.Loss of TRPA1 suppressed expression of TGFb1 and substance P in response to epithelial debridement, but not of IL-6.
TRPA1 receptor-signal is required for healing of an epithelial debridement in association with suppression of cell proliferation and of up-regulation of gene expression of TGfb1 and substance P in mice.
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