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Takayoshi Sumioka, Yuka Okada, HIroki Iwanishi, Shingo Yasuda, Masayasu Miyajima, Shizuya Saika; Impaired angiogenic response in cornea by lacking TRPV4 in mice. Invest. Ophthalmol. Vis. Sci. 2019;60(9):949.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the effects of loss of transient receptor potential vanilloid 4 (TRPV4) in the development of neovascularization in a corneal stroma in mice. TRPV4 is a cation channel type receptor involved in febrile hyperalgesia and pain as well as multiple cell behavior modulation as a mechanosensor.
(1) Corneal neovascularization from the limbal vessels was induced by cauterization of the central cornea of an eye of both C57BL/6 (WT) mice (n = 24) and TRPV4-null (KO) mice (n = 25) by a disposable tool of Accu-temp. The eye was processed for cryosectioning and were examined by using immunohistochemistry. Expression of angiogenic growth factors and inflammatory cell markers were examined in RNA samples derived from day 3 tissues and uninjured ones by using TaqMan real time-RT-PCR. (2) We employed in vitro assay of angiogenic activity of human umbilical vein endothelial cell (HUVEC). The culture was maintained in the routine culture condition in the presence of VEGF-A as an angiogenesis inducer in the presence or absence of a TRPV4 antagonist (HC-067047). The length of tube-like structure formation was compared and examined after 12 hours.
(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. Expression of mRNAs of F4/80 macrophage antigen was significantly less in a KO cornea as compared with a WT cornea at day 3. (2) The angiogenic activity in HUVEC was significantly suppressed by the addition of TRPV4 antagonist in a concentration-dependent manner.
TRPV4 signal is involved in macrophage infiltration and angiogenesis process in a mouse cornea.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
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