Figure 1.

Corneal perforating incision injury induces transient edema and results in isolated lymphangiogenesis without hemangiogenesis. (A) Mouse model of central perforating corneal incision injury. After application of atropine to dilate the pupil and avoid iris incarceration, a linear perforating corneal incision (1.0 mm length) is performed (dashed lines). The lens and iris are not touched. Ac: anterior chamber; co: cornea; ir: iris; le: lens; pu: pupil; sc: sclera. (B–E) In vivo optical coherence tomography scans of the anterior segment demonstrate a transient increase of corneal thickness as a measure of corneal edema; green bars: areas of corneal thickness measurements; green values: central corneal thickness. (F–I) Corneal whole mounts stained with LYVE-1 (red) and CD31 (green); dashed lines: area of incision injury. LYVE-1^high/CD31^low lymphatic vessels (arrows) growing towards the central cornea are detectable 1 week after injury and persist until 2 weeks after injury. Afterwards, lymphatic vessels regress and the area covered by lymphatic vessels after 4 weeks is comparable to uninjured corneas. In contrast to lymphatic vessels, no significant ingrowth of LYVE-1^neg/CD31^high blood vessels into the cornea is detectable; p.i.: post injury. (J–K) Quantification of corneal lymph- and hemangiogenesis; data are shown as mean + SD; n = 5–10 per time point; statistical analysis was performed using the unpaired 2-tailed Student’s t test: ***: p < 0.001; n.s.: not significant.