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Takayoshi Sumioka, Yuka Okada, Osamu Yamanaka, Yuka Nidegawa, Masayasu Miyajima, Ken-ichi Matsumoto, Shizuya Saika; Relation of Tenascin X and VEGF in the corneal cauterization model. Invest. Ophthalmol. Vis. Sci. 2016;57(12):3525.
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© ARVO (1962-2015); The Authors (2016-present)
To examine the deposition pattern of tenascin X (TNX) and VEGF-A or B in the corneal stroma after cauterization in the C57BL/6 (WT) mice. Loss of TNX in cultured macrophage attenuates VEGF expression in vitro (ARVO2015). We also here examined cauterization-induced cornea neovascularization in mice in the earlier and later stages, although we previously reported less neovascularization in TNX-null mice at day 7 in this model (ARVO 2014).
Corneal neovascularization from the limbal vessels was induced by cauterization of the central cornea of an eye of both WT mice (n = 45) and KO mice (n = 47) by disposable tool of Optemp. Mice were killed at day 3, 7 and 14. The eye was then enucleated, processed for cryosectioning and paraffin section and were examined by using double-immunostaining for TNX and VEGF-A or B or for CD31.
TNX was only detected in the corneal stroma near limbus in a WT cornea under the uninjured condition. TNX was expressed at the same deposition of VEGF-A or B in the corneal stroma of central and limbus at day 3, 7 and 14 after cauterization. The deposition of VEGF-A or B was less in a KO cornea as compared with a WT cornea. The length of the neovascularization from the limbus was similar between genotypes of mice at day 3 and 14, although was less in a KO cornea as compared with a WT cornea at day 7.
Cauterization-induced upregulation of TNX was associated with expression of VEGF-A or B in the corneal stroma in mice. The inhibitory effect of the loss of TNX on corneal neovascularization was revealed to be transient.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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