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K. Ishikawa; Role of Mip-1β in Mouse Model of Oxygen-Induced Retinopathy. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4461.
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We previously reported that the gene expression level of Macrophage inflammatory protein-1β(MIP-1β), a member of CC chemokine subfamily which may play a role in the recruitment of macrophages, was significantly up-regulated in the ischemic retinas of mouse model of oxygen induced retinopathy using gene microarray analyses. The aim of this study was to examine expression time course, localization and function of MIP-1β in the model.
C57BL/6N pups were placed in a 75% oxygen environment on postnatal day 7 for 5 days and then returned to room air. Retinas were removed from mice at 0,3,6,12 hours (h),1,2,3,and 5 days after relative ischemia. Total RNA and protein were extracted from each retina, and the expression levels of MIP-1β were measured by real-time quantative PCR and ELISA method. The localization was examined by immunohistochemstry and laser capture microdissection. The number of F4/80 positive cells and mRNA expression levels of F4/80 were measured in the P17 whole retinas after administration of the neutralizing antibodies against MIP-1β.
MIP-1β mRNA levels increased at 6 h and maximal at 12 h after ischemia. MIP-1β protein levels were also increased at 12 h and maximal at 2 days after ischemia. Immunohistochemistry demonstrated that MIP-1β was localized in the ganglion cell layer and the inner nuclear layer. Administration of the neutralizing antibodies against MIP-1β decreased levels of F4/80 mRNA expression and the number of infiltrating F4/80 positive cells(p<0.05, n=8).
MIP-1β was expressed in the hypoxic inner retina in the mouse model of oxygen induced retinopathy. Our data suggest that MIP-1β may play a role in the inflammation induced by the ischemic retinopathy.
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