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. 2023 Jan 24;64(1):19. doi: 10.1167/iovs.64.1.19

Figure 3.

Figure 3.

Loss of the TRPM8 function accelerates the speed of corneal epithelial wound healing, and TRPM8 activation delays epithelial repair. Corneal epithelium debridement (2.5-mm diameter) was performed at hour 0. Wound healing progress was observed by performing fluorescence staining for epithelial defects and was photographed with a slit lamp microscope after debridement. (A) Experimental schematic diagram of the effect of TRPM8 deficiency on corneal wound healing. (B) Epithelial wound healing progress in Trpm8−/− and WT mice. (C) Comparison of defect area/total cornea (%) between Trpm8−/− and WT groups (n = 5 per group) at different times. (D) Ki67 staining of corneal sections. The arrowhead indicates the limbus. Epi, epithelium; Str, stroma. Scale bar, 100 µm. (E) Comparison of Ki67-positive cell numbers (within cornea range of 400 µm from the limbus; n = 4 per group). (F) Experimental schematic diagram of the effect of TRPM8 activation on corneal wound healing. (G) Epithelial wound healing progress in WT mice treated with menthol or vehicle solution. (H) Comparison of defect area/total cornea (%) between control and menthol groups (n = 5 per group) at different times. ns, means no significance; *P < 0.05, ** P < 0.01, ***P < 0.001.