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S. Yoshida, A. Yoshida, T. Ishibashi, S.G. Elner, V.M. Elner; MCP–1 and MIP–1alpha Expression in Retinal Neovascularization during Postischemic Inflammation in a Mouse Model of Ischemic Retinopathy . Invest. Ophthalmol. Vis. Sci. 2004;45(13):477.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Macrophages are important participants in neovascularization. This study was designed to examine the role of the monocyte/macrophage chemotactic proteins, monocyte chemotactic protein–1 (MCP–1), and macrophage inflammatory protein–1alpha (MIP–1alpha) in a mouse model of oxygen–induced ischemic retinopathy and to determine whether the morphology and distribution of macrophages/microglia are concomitantly altered. Methods: C57BL/6J pups were placed in a 75% oxygen environment on postnatal day 7 (P7) for 5 days and then returned to room air. Northern blot analysis and ELISA were performed to examine the expression levels of MCP–1 and MIP–1alpha in the retinas after ischemia. To determine the cellular source of the chemokines, serial sections of retinal tissues were subjected to in situ hybiridization. Results: The MCP–1, MIP–1alpha mRNA levels increased at 3 h after ischemia. MCP–1, MIP–1alpha, and vascular endothelial growth factor protein levels were also increased markedly. Immunostaining demonstrated that the macrophages/microglia in the retina had morphological changes with enlarged processes, and some were closely associated with neovascular tufts at postnatal day 17. Coadministration of the neutralizing antibodies against MCP–1 and MIP–1alpha inhibited retinal neovascularization by 30%. Conclusions: Our data suggest that chemokines are involved in the induction of retinal neovascularization and play a role in the inflammation induced by the ischemic retinopathy, possibly by modulating or attracting macrophages/microglia.
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