At present, the only treatment for glaucoma is intraocular pressure control. We know some people still get worse despite good pressure control. We have evidence that a system previously only thought to modulate blood pressure control has an important role in halting glaucoma damage. Furthermore, there has been a recently described new component of this system that may play a greater role in this process. This new part of the system has never been comprehensively described in the human eye. We would like to examine this system further in the human eye using molecular biological techniques.
The renin-angiotensin system (RAS) is distributed ubiquitously in the eye. Angiotensin I is converted to Angiotensin II via Angiotensin Converting Enzyme (ACE). Angiotensin II acts at specific receptors in the eye (AT1R and AT2R). Stimulation of AT1R can cause increased cell death in a glaucoma model.
However, downstream from AT1R and AT2R is a neuropeptide based system that acts at the receptor MAS in an antagonistic fashion to AT1R. It has only very recently been described in the cardiovascular literature and is dependent on the enzyme ACE2. This system can be modulated in the eye by water soluble agents already FDA approved.
The aim of this project is to characterise this new ACE2 dependent downstream pathway in the human eye which has never been described fully here before and look for targets that can be modulated to confer neuroprotection suitable for clinical trial.
We aim to examine this ACE2 dependent system in human cadaveric donor eyes from the Sydney Eye Bank utilising histological and immunofluorescence techniques as well as Real Time PCR. This project involves collaboration with colleagues at the University of NSW.
The opportunity ID for this research opportunity is 1826