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Takayoshi Sumioka, Yuka Okada, Osamu Yamanaka, Masayasu Miyajima, Ken-ichi Matsumoto, Shizuya Saika, HIroki Iwanishi; Impairment of cornea epithelial wound healing in a Tenasin X-deficient mouse. Invest. Ophthalmol. Vis. Sci. 2018;59(9):4353.
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© ARVO (1962-2015); The Authors (2016-present)
To examine if tenascin X (TNX) gene deletion affects healing of an epithelial injury in a mouse cornea.
A round epithelial defect were produced in TNX -/- (KO, n =15) and C57BL/6 (WT, n=15) mice by using a 2mm trephine and surgical blade. (1) At healing intervals of up to 36 hrs, each cornea was photographed with green fluorescein staining and the remaining epithelium defect was evaluated. (2) The healing eyes were enucleated, processed for paraffin section and examined by using histology and immunohistochemistry. (3) Healing corneas of both genotypes of mice were processed for observation of corneal nerves in a flat-mount preparation.
(1) At 12, 18 and 24 hrs, but not at 36 hrs, post-debridement, the remaining defect in KO mice was statistically significantly larger than that in WT mice. (2) Absence of TNX suppressed the expression of Interleukin-6 in healing epithelium and infiltration of neutrophils in to the stroma in response to epithelial debridement. (3) There was no difference in the regeneration of the sensory nerve in the healing cornea between WT and KO mice.
TNX is required for the healing of debrided corneal epithelium in mice. TNX could be involved in the process of minor inflammation critical for epithelial repair. Loss of TNX did not affect corneal nerve regeneration although TNX was reportedly involved in nerve maintenance.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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