Purchase this article with an account.
T. Usui, K. Sugisaki, S. Yokoo, S. Yamagami, S. Amano, N. Nagai, S. Ishida; Inhibition of Corneal Neovascularization by Blocking the Angiotensin II Type 1 Receptor. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1715.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To examine whether the angiotensin II type 1 receptor (AT1-R) signaling plays a role in corneal neovascularization
Corneal neovascularization was induced by suturing 10-0 nylon 1 mm away from limbal vessel in C57BL/6 mice. The expression of angiotensin II and AT1-R was evaluated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR), in situ PCR, and immunohistochemistry. To investigate the function of angiotensin II signalling in inflammatory corneal neovascularization, Telmisartan (AT1-R antagonist) or PBS (control) was administered intraperitonelly and neovascularized area was compared between control and treated mice.
Angiotensin II and AT1-R mRNA and protein markedly increased in the neovascularized corneas compared with normal corneas. Neovascularized area in cornea of Telmisartan-treated mice was significantly small compared with that of control mice on day 7 after corneal suture.
AT1-R signaling inhibition by Telmisartan significantly attenuates corneal neovascularization, suggesting that termisartan may be a therapeutic target for suppression of corneal neovascularization.
This PDF is available to Subscribers Only