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Takayoshi Sumioka, Yuka Okada, Yuka Nidegawa, Masayasu Miyajima, Kenichi Matsumoto, Shizuya Saika; Impaired angiogenic response in cornea by lacking tenascin X in mice. Invest. Ophthalmol. Vis. Sci. 2014;55(13):3237.
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To investigate the effects of loss of TNX in the development of neovascularization in a corneal stroma in mice. Tenascin X (TNX) is one of the wound healing-related matrix macromolecules, and reportedly binds to vascular endothelial growth factor and accelerates the growth of vascular endothelial cells.
Corneal neovascularization from the limbal vessels was induced by cauterization of the central cornea of an eye of both C57BL/6 (WT) mice (n = 60) and TNX-null (KO) mice (n = 60) by disposable tool of Optemp. Mice were killed at day 3 and 7. (1) The eye was then enucleated, processed for cryosectioning and paraffin section and were examined by using immunohistochemistry. (2) Expression of angiogenic growth factors and inflammatory cell markers were examined in RNA samples derived from day3 corneal samples and uninjured corneas by using TaqMan real time-RT-PCR.
(1) The length of the neovascularization from the limbus was less in KO mice as compared with WT mice at day 7 as revealed by CD31 immunostaining. (2) Expression of mRNAs of VEGF, F4/80 macrophage antigen and α-smooth muscle actin (αSMA) was significantly less in a KO cornea as compared with a WT cornea under the uninjured condition, and that of F4/80 and αSMA was significantly less in a KO cornea as compared with a WT cornea at day 3 posty-cautarization.
TNX is involved in macrophage infiltration and VEGF expression in the cornea. Endogenous TNX modulates expression of angiogenic cytokines and involved in development of corneal neovascularization.
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