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Katsuo Tomoyose, Yuka Okada, Takayoshi Sumioka, Kumi Shirai, Shizuya Saika; Impaired angiogenic response in cornea by lacking TRPV1 in mice. Invest. Ophthalmol. Vis. Sci. 2013;54(15):2092.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the effects of loss of Transient receptor potential (TRP)V1 in the development of neovascularization (NV) in a corneal stroma in mice. TRP channels are polymodal receptors that are activated by a host of stimuli to mediate sensory transduction.
Corneal NV from the limbal vessels were induced by cauterization of the central cornea of an eye by using disposable tool of Optemp. WT and TRPV1-null (KO) mice (n = 16 in each genotype) were used and killed at day 3 and 7. The eye was enucleated and processed or cryosectioning for histology and immunohistochemistry. To examine the expression of angiogenic growth factors in vivo, centrally cauterized cornea (n = 40 in each of WT or KO group) was excised at day 3. Total RNA was extracted from samples and processed for real-time RT-PCR for VEGF, TGFb1.
The development of CD31-labeled new vessels from the limbus toward the center of the cornea was impaired in KO mice as compared with WT mice at day 3 days, but not at day 7. Expression of mRNAs of VEGF and TGFb1 was significantly less in a KO cornea as compared with a WT cornea at day 3.
TRPV1 signal is involved in the development of cauterization-induced NV in corneal strom via modulation of angiogenic gene expression in the affected tissue.
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