Fig. 5

ATSE-induced impairment of corneal wound healing requires NF-κB signaling. a Relative NF-κB expression using mRNA isolated from whole wounded corneas of the RA, ATSE, and ATSE + 6-OHDA groups at 6, 12, 18, and 24 h after corneal abrasion (one-way ANOVA, Tukey's post hoc test, RA vs. ATSE, *p < 0.05, **p < 0.01, ***p < 0.001; RA vs. ATSE + 6-OHDA, ^##p < 0.01, ^###p < 0.001, n = 4). b Representative open corneal wounds (revealed by topical fluorescein) and visible wound closure over time post wounding. c Percent decrease in open wound area over time after wounding (two-way RM ANOVA, interaction p = 0.00002, Bonferroni’s multiple comparisons test, n = 6 corneas per time point per group). d Dividing epithelial cells over time post-wounding (two-way ANOVA, interaction p = 0.0278, Sidak’s multiple comparisons test, n = 6 corneas per time point per group). e Neutrophil influx into the cornea over time after corneal abrasion (two-way AVOVA, interaction p < 0.0001, Sidak’s multiple comparisons test, n = 6 corneas per time point per group). f γδ T cell influx into wounded corneas over time (two-way ANOVA, interaction p = 0.0020, Sidak’s multiple comparisons test, n = 6 corneas per time point per group). * comparison between ATSE and RA treatments in wild-type mice; ^# comparison between ATSE-treated wild-type mice and ATSE + Nfkb1-mutated animals. *^{, #} denote p < 0.05, **^{, ##}p < 0.01, and ***^{, ###}p < 0.001, comparing groups as indicated