Fig. 4: Activation of the GAS6-MERTK pathway decreases pathological angiogenesis in the OIR model.
A Myeloid SOCS3-deficient (LysM-Cre SOCS3fl/fl) mice or control (SOCS3fl/fl) littermates were subjected to OIR protocol, injected at P14 intravitreally in the right eye with MerTK-Fc chimera protein, and in the left eye with IgG1 Fc, and sacrificed at P17. The number of epiretinal neovascular nuclei in PAS-stained retinal cross-sections is shown. (n = 14–18 mice). B Primary microglia were treated with 62 ng/ml recombinant GAS6 for 30 min, followed by a co-incubation with pHrodo-labeled apoptotic HUVECs. Phagocytosis rate was recorded for 3 h with 10 min intervals, and quantified by calculating the mean number of pHrodo particles per microglia. (n = 5 microglia cell isolations). C C57BL/6 J mice were subjected to OIR, injected at P14 intravitreally in the right eye with recombinant GAS6 protein, and in the left eye with vehicle (PBS), and sacrificed at P17. A number of epiretinal neovascular nuclei in PAS-stained retinal cross-sections are shown. (n = 23 mice). (D) C57BL/6 J mice were subjected to OIR, injected at P14 intravitreally in the right eye with recombinant MFGE8 protein, and in the left eye with vehicle (PBS), and sacrificed at P17. A number of epiretinal neovascular nuclei in PAS stained retinal cross-sections is shown. (n = 9 mice) Data are presented as mean ± SEM, *p < 0.05, **p < 0.01.
