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Increased Expression of Chemokine KC, an Interleukin-8 Homologue, in a Model of Oxygen-Induced Retinopathy

Purpose: The purpose of this study was to determine the retinal expression of angiogenic chemokines/cytokines in a mouse model of oxygen-induced retinopathy. Methods: C57BL/6 (B6) mice were exposed to 75% oxygen from postnatal day 7 (P7) to P12 and then recovered in room air. Reverse transcription–polymerase chain reaction (RT-PCR) was used to determine relative mRNA levels of KC, macrophage inflammatory protein-2 (MIP-2), interleukin-1α (IL-1α), and interferon gamma (IFN-γ). Immunohistochemistry was used to localize KC in the retina. IL-1α was also injected into the vitreous of mouse eyes, and KC expression was examined by RT-PCR, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry. Results: KC expression at both the mRNA and protein levels was increased in P14, P17, and P21 of hyperoxia-injured eyes. KC immunoreactivity was localized along the nerve fiber layer and in radial Müller cell processes. IL-1α mRNA was modestly increased in hyperoxia-injured eyes on P14 and P17. INF-γ mRNA was not detected in the retina. Adult mouse eyes injected with IL-1α demonstrated increased levels of both KC mRNA and protein, with KC immunoreactivity localized to Müller cell processes. Conclusions: Oxygen-induced injury to the developing retina results in the induction of the CXC chemokine KC at both the mRNA and protein levels during the peak time points of neovascularization, suggesting a possible role in the pathogenesis of retinopathy of prematurity.