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T. Sumioka, A. Kitano, N. Fujita, Y. Okada, M. Miyajima, S. Saika; Impaired Angiogenic Response in Cornea by Lacking Tenascin C in Mice. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2034.
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© ARVO (1962-2015); The Authors (2016-present)
Tenascin-C (TNC) is one of the wound healing-related matrix macromolecules that is usually temporary upregulated in an injured tissue like fibronectin. To investigate the effects of loss of TNC in the development of neovascularization in a corneal stroma in mice.
Corneal neovascularization from the limbal vessels were induced by cauterization of the central cornea of an eye by disposable tool of Optemp. One eye of both WT and KO mice (n = 12 in each genotype) were treated and killed at day 3, 7 and 14. The eye was then enucleated and processed or cryosectioning. Each genotype corneas were used for histology at each timepoint as described below.To examine the expression of angiogenic growth factors and inflammatory cell markers in vivo, centrally cauterized cornea (n = 6 in each of WT or KO group) was excised at day 3 and 7. Total RNA was extracted from cauterized tissue and processed for real-time RT-PCR for VEGF, TGFb1, F4/80 macrophage antigen and myoloperoxidase (MPO) .
The length of the neovascularization was less in KO mice as compared with WT mice at day 3 and day 7, but not at day 14. Expression of mRNAs of both VEGF and TGFb1 was significantly less in a KO cornea as compared with a WT cornea at day 3, but such difference was not detected at day 7. Expression of F4/80 was suppressed by the loss of TNC at day 3, but not at day 7. Expression of MPO was not significantly affected by gene ablation of TNC.
TNC is involved in angiogenic gene expression and is required for neovascularization in corneal stroma.
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