April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
Role of MIP-1β in a Mouse Model of Oxygen Induced Retinopathy
Author Affiliations & Notes
  • K. Ishikawa
    Kyushu University, Fukuoka, Japan
  • Footnotes
    Commercial Relationships  K. Ishikawa, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 4138. doi:
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      K. Ishikawa; Role of MIP-1β in a Mouse Model of Oxygen Induced Retinopathy. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4138.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : 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 and localization of MIP-1β in the model.

Methods: : 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 microdissections.

Results: : 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.

Conclusions: : 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.

Keywords: retinal neovascularization 

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