Fig. 4

Impact of ETs on retinal and vascular repair upon laser-induced injury. a, b Kinetics of retinal injury detected in reflectance (back-scattered light) in untreated, GM-CSF1 KO, Cx3cr1^gfp/gfp and PAD4 inhibitor-treated mice. a Image of the same area after laser on days 1, 4 and 7 in PAD4 inhibitor-treated mice. We detected a reduction of hypo-/hyper-reflectivity in the damaged site on day 4, and no signal was found by day 7. b Quantification of the damaged area of untreated, GM-CSF1 KO, Cx3cr1^gfp/gfp and PAD4 inhibitor-treated retinas after injury (day 0) and at pre-defined time points (day 1, 4, 7, 10 and 14). Significant differences (*p < 0.1, **p < 0.01 and ****p < 0.0001) between untreated, GM-CSF1 KO, Cx3cr1^gfp/gfp and PAD4 inhibitor-treated mice were determined by using a post-hoc Bonferroni one-way ANOVA test (n = 8). c Representative fluorescein angiographs of the same PAD4 inhibitor-treated eyes on days 1, 4 and 7. d Quantification of dye that leaks in the depth of the retina, identified as leakage area, after injury (day 0) and at pre-defined time points (day 1, 4, 7, 10 and 14). Significant differences (*p < 0.1, **p < 0.01, ***p < 0.001 and ****p < 0.0001) between untreated, GM-CSF1 KO, Cx3cr1^gfp/gfp and PAD4 inhibitor-treated mice were determined by using a post-hoc Bonferroni one-way ANOVA test (n = 8). For both groups, day 0 was chosen as calibrator [NRQ (normalized relative quantification) = 1]. Field of view is approximately ≈ 425 µm