Figure 2.

Mouse model of OIR. A) A schematic diagram depicting the mouse OIR procedure. Neonatal mice and their nursing mother are exposed to 75% oxygen from P7 to 12. Excessive oxygen suppresses the development of the retinal vasculature and leads to regression of the existing immature retinal vessels, which results in a central zone of vaso-obliteration. At P12, mice are returned to room air, and the relative hypoxia triggers both normal vessel regrowth toward the vaso-obliteration zone and pathologic retinal neovascularization at the border between the vascular and avascular zones, which also protrude toward the vitreous space. The levels of neovascularization reach maximum severity at P17. B) Representative images of retinal flat mounts with isolectin staining in the normoxic and OIR retinas show the normal retinal vasculature at P7 (left), vaso-obliteration at P12 (middle; the vessel loss area is highlighted with white outline), and pathologic neovascularization at P17 (right; the vessel loss area is highlighted with white dashed line). Scale bar, 1 mm. C) Magnified images of isolectin-stained retinal flat mounts show the normal retinal vasculature from normoxic retinas (left) and abnormal neovessels from OIR retinas (right; image enlarged from the rectangular white box region in panel B at P17). D) Cross-sections of mouse retinas with normoxia (left) and OIR (right) at P17. Preretinal neovascular tufts (arrowheads) arise from the superficial retinal vascular layer of the OIR retina and protrude into the vitreous space. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; ONL, outer nuclear layer; OPL, outer plexiform layer.