Purchase this article with an account.
B. E. Goldhagen, A. D. Proia, P. V. Rao; Elevated Levels of RhoA in the Optic Nerve Head of Human Eyes With Glaucoma. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2191. doi: https://doi.org/.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Rho GTPase and its downstream kinase effector Rho kinase (ROCK-1 and ROCK-2) play a critical role in regulating aqueous humor outflow, and inhibition of these proteins decreases intraocular pressure in humans. In this study, we evaluated changes in the expression profile of RhoA, ROCK-1, and ROCK-2 in the aqueous humor outflow pathway and optic nerve head of human eyes with or without glaucoma to explore their potential involvement in glaucoma pathophysiology.
Age-matched paraffin-embedded postmortem eyes from patients with or without glaucoma were stained immunohistochemically using polyclonal antibodies raised against RhoA, ROCK-1, and ROCK-2. The intensity of the immunostaining in the aqueous humor outflow pathway and the optic nerve head was graded by four individuals who were masked concerning whether the eyes were from normal individuals or those with glaucoma.
In both normal eyes and those with glaucoma we observed RhoA, ROCK-1, and ROCK-2 in the trabecular meshwork, ciliary muscle, and optic nerve head with sparing in the scleral spur. There was a significant increase in the RhoA protein levels in the glaucomatous optic nerve head compared to the age-matched controls. Conversely, there was decreased RhoA/ROCK expression in the glaucomatous eye aqueous humor outflow pathway.
Elevated levels of RhoA in the optic nerve head of glaucomatous eyes indicate potential involvement of RhoA in the pathophysiology of glaucoma. We speculate that the trend towards a decreased RhoA/Rho kinase expression in the aqueous outflow pathway may be the result of medications being used to control the patients’ glaucoma.
This PDF is available to Subscribers Only