Impaired Angiogenic Response in the Corneas of Mice Lacking Osteopontin

被引:22
作者
Fujita, Norihito [1 ]
Fujita, Shuko [1 ]
Okada, Yuka [1 ]
Fujita, Kyoko [1 ]
Kitano, Ai [1 ]
Yamanaka, Osamu [1 ]
Miyamoto, Takeshi [1 ]
Kon, Shigeyuki [2 ]
Uede, Toshimitsu [2 ]
Rittling, Susan R. [3 ]
Denhardt, David T. [3 ]
Saika, Shizuya [1 ]
机构
[1] Wakayama Med Univ, Dept Ophthalmol, Wakayama 6410012, Japan
[2] Hokkaido Univ, Inst Med Genet, Div Mol Immunol, Sapporo, Hokkaido, Japan
[3] Rutgers State Univ, Dept Cell Biol & Neurosci, Piscataway, NJ USA
关键词
CELL-MEDIATED-IMMUNITY; ALKALI BURNS; NEOVASCULARIZATION; MOUSE; BONE; INFLAMMATION; FIBROSIS; DISEASE; MATRIX; CANCER;
D O I
10.1167/iovs.09-3420
中图分类号
R77 [眼科学];
学科分类号
100212 [眼科学];
摘要
PURPOSE. To investigate the effects of loss of osteopontin (OPN) in the development of neovascularization in corneal stroma in mice. Cell culture study was also conducted to clarify the effects of OPN in transforming growth factor (TGF) beta 1-driven cell signaling and expression of vascular endothelial growth factor (VEGF). METHODS. Ocular fibroblasts from wild-type and OPN-null mice were used to study the role of OPN in TGF beta 1 signal and VEGF expression. The effect of the absence of OPN on corneal neovascularization was evaluated in mice. RESULTS. In ocular fibroblast culture, loss of OPN attenuated TGF beta 1 signals (Smad3 and p38) and reduced expression of VEGF. Loss of OPN attenuated neovascularization in corneal stroma in mice. CONCLUSIONS. OPN is involved in VEGF expression in cultured fibroblasts and is required for neovascularization in corneal stroma in vivo. (Invest Ophthalmol Vis Sci. 2010; 51: 790-794) DOI: 10.1167/iovs.09-3420
引用
收藏
页码:790 / 794
页数:5
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