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(Investigative Ophthalmology and Visual Science. 2007;48:3545-3550.)
© 2007 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.06-0695
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Role of Macrophage Migration Inhibitory Factor in Corneal Neovascularization

Tomohiko Usui,*,1 Satoru Yamagami,*,1 Shuichi Kishimoto,1 Yokoo Seiich,1 Toshinori Nakayama,2 and Shiro Amano1

1From the Department of Ophthalmology, Faculty of Medicine, University of Tokyo, Tokyo Japan; and the 2Department of Molecular Immunology and Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.

PURPOSE. To determine the role of macrophage migration inhibitory factor (MIF) in inflammatory corneal neovascularization.

METHODS. Corneal neovascularization was induced by suturing 10-0 nylon 1 mm away from limbal vessel or limbal scraping after 0.15 M NaOH application in BALB/c mice. MIF expression was evaluated by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR), Western blot analysis, and immunohistochemistry. To investigate the function of MIF in inflammatory corneal neovascularization, the neovascularized area and number of infiltrating F4/80-positive cells (monocytes/macrophages) were compared between wild-type mice and homozygous MIF-deficient mice.

RESULTS. MIF mRNA and protein markedly increased in the neovascularized corneas compared with normal corneas by RT-PCR and Western blot analysis, respectively. MIF expression was upregulated immunohistochemically, not only in the corneal epithelium but also in the stromal infiltrating cells of neovascularized corneas. Neovascularized area in corneas of MIF–/– mice was significantly small compared with that in wild-type mice on day 7 after corneal suture and on day 14 after limbal scrape, and MIF–/– cornea had ~30% less neovascularized area than did wild-type cornea in both models. Neovascularized corneas in MIF-deficient mice had significantly fewer monocytes/macrophages than those in wild-type control mice.

CONCLUSIONS. These findings indicate that MIF, abundantly expressed in neovascularized corneas, has an angiogenic role in inflammatory corneal neovascularization and may be a therapeutic target for suppression of corneal neovascularization.




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H. Mochimaru, T. Usui, T. Yaguchi, Y. Nagahama, G. Hasegawa, Y. Usui, S. Shimmura, K. Tsubota, S. Amano, Y. Kawakami, et al.
Suppression of Alkali Burn-Induced Corneal Neovascularization by Dendritic Cell Vaccination Targeting VEGF Receptor 2
Invest. Ophthalmol. Vis. Sci., May 1, 2008; 49(5): 2172 - 2177.
[Abstract] [Full Text] [PDF]


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