Fig. 2. The absence of synd1 leads to delayed closure of corneal epithelial scrape wounds, which is associated with a failure to increase cell proliferation after wounding. The numbers of open wounds and corneas used to generate these data are presented in the methods section. (A) Representative photomicrographs obtained after wounding at the indicated times (d, day) are depicted. The delay in closure of epithelial wounds is statistically significant (P<0.05) at 24 and 36 hours (asterisk) as determined using the Mantel-Haenszel Chi-Squared test. (B) Data from the experiment described in A were used to create a graph showing the time (hr, hour) of 50% wound closure. There is an 8-hour delay in the 50% wound closure time in synd1ko mice compared with wild-type mice. (C) Cell proliferation was assessed using BrdU. Data show that, although wild-type corneal epithelial cells increase proliferation at 24 hours after wounding, the synd1ko animals fail to respond to the corneal wound by increasing their proliferation rate at any time point analyzed. Data for the synd1ko are significantly (P<0.05) different from wildtype at 24 hours. Surprisingly, there is also a significant (P<0.05) increase in proliferation rate in the unwounded synd1ko mice compared with that in unwounded wild-type mice. Data are compared using the unpaired t-test, and asterisks indicate significant differences between groups. (D) Histology shows that migration in the synd1ko mouse cornea is associated with a transient increase in inflammatory cells in the corneal stroma and a failure to restratify properly by 2 weeks. 18 hours after wounding, more inflammatory cells are observed beneath the migrating synd1ko epithelial sheet than in the wildtype. Arrows indicate the leading edge, and the arrowheads indicate inflammatory cells; direction of cell migration is from left to right. Bar, 60 µm.

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