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N. Fujita, S. Fujita, K. Fujita, Y. Okada, K. Ikeda, S. Kon, S. R. Rittling, D. T. Denhardt, M. Miyajima, S. Saika; Suppression of Corneal Neovascularization and TGF-Beta Signal in Osteopontin-Null Mice. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1482.
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To examine the effect of lacking osteopontin (OPN), a multi-potential extracellular matrix component, for angiogenic activity in cornea wound healing. Effects of lacking OPN on TGFbeta signal were also examined.
Neovascularization in the peripheral corneal stroma was induced in wild type (WT) and OPN-null (KO) mice by cauterization at the central cornea. Cryosection was immunohistochemically examined at day 3, 7, and 14. The length of new vessels in the stroma from the anterior chamber angle was measured. Ocular fibroblast outgrowth from post-natal day 1 eyeball shell of WT and KO mice. Confluent cells were exposed to TGFbeta1 and activated cytoplasmic signaling, i. e., Smad, p38 or JNK, was analyzed by western blotting.
Loss of OPN suppressed cauterization-induced neovascularization in the peripheral stroma up to day 14. The length of new vessels in the stroma from the anterior chamber angle was 0.164 (+/-0.096) mm in KO mice and the length of wild type was 0.478 (+/-0.193) mm in WT mice at day 7. Loss of OPN attenuated TGFbeta1-activated Smad3 and p38 MAP kinase.
Lacking OPN suppresses cauterization-induced corneal neovascularization. Loss of this molecule attenuates TGFbeta signal in ocular fibroblasts.
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