Figure 4.

Axon density improves at similar rates at the center of SDC1-null and WT corneas after 1.5-mm debridement wounds. (A) Corneas from WT and SDC1-null mice injured by 1.5-mm debridement wounding are stained with an antibody against βIII tubulin to visualize the ICNs. Representative images from adult male WT and SDC1-null mouse corneas at 1 and 28 days after debridement wounding are shown. (B) Images including those presented in (A) were used to quantify the axon density of the ICNs using Sholl analysis at 1, 2, 3, 4, 7, 14, and 28 days after debridement. Data are normalized relative to unwounded controls for each genotype. Asterisks within bars indicate significant differences in axon density relative to unwounded controls. (C) Axon thickness was assessed at the center and periphery 2, 3, 14, and 28 days after debridement wounding in WT and SDC1-null corneas. Data have been normalized relative to unwounded mice. Asterisks within bars indicate significant differences in axon thickness relative to unwounded controls. Data show that normalized axon thickness decreases significantly relative to controls at 2 and 3 days in the center of SDC1-null corneas and at 2, 3, 14 days in the center of WT corneas. At the periphery in SDC1-null mice, normalized axon thickness is similar to controls at 14 and 28 days but lower than controls at 2 and 3 days. At the periphery in WT mice, normalized axon thickness is lower than control at 2 and 14 days but similar to controls at 3 and 28 days. Scale bar in (A): 250 μm.