Mouse model of oxygen-induced retinopathy

The procedures to produce the oxygen-induced retinopathy model were based on the previously described method of Smith et al.⁵⁰. On postnatal day (P) 7, mouse pups and the nursing mother were placed in an airtight incubator (own production) ventilated by a mixture of oxygen and air to a final oxygen fraction of 75% ± 2%. The oxygen levels were checked at least three times per day. After five days of hyperoxia, these mice were returned to room air at P12. The OIR model comprises two critical stages of vascular pathologic process. During the first phase of hyperoxic exposure (P7-P12), immature retinal vessels regressed and the development of the normal retinal vasculature was delayed, leading to a central zone of vaso-obliteration (VO). After returning mice to room air at P12, the central avascular retina becomes relative hypoxic, triggering both normal vessel regrowth, which predominantly occur within the VO with relative normal shape of vasculature before P14, and a pathologic formation of extraretinal neovascularization, which occurred at the border of VO and periphery retinal vasculature after P14 with the maximum severity at P17. In this study, the central avascular area was measured at P12 and P14. Some C57/B6 mice at P7 received a single intravitreal injection of IL-17 neutralizing antibody (2 μg/eye, R&D systems) and were then used to establish the OIR model.