Postgraduate Research Student
- 2001-date: Postgraduate Research Student, School of Biotechnology, Dublin City University.
- 1998-1999: Research Assistant, Irish Center for Colloid Science and Biomaterials, University College Dublin.
- 1994-1998: B.Sc. in Biotechnology, School of Biotechnology, Dublin City University.
- 1997: Research Assistant, GlaxoWellcome, Beckenham, England.
Ongoing Research
- Retinal
endothelial and pericyte cell responses to mechanical stimuli
Glaucoma is the second leading cause of blindness in the developed world. The disease is characterized by a progressive loss of visual field and an alteration in the appearance of the optic nerve head. Raised 'intra-ocular pressure' or IOP is recognized as a leading factor causing the disease, however many people with glaucomatous damage have IOP values within the normal range (termed 'Normal Tension Glaucoma' or NTG).
Vascular factors have been implicated in NTG. Incidences of systemic hypotension, vasospasm, cold hands and feet are higher than in normal subjects, implying that ischemia is responsible for the damage to the optic nerve head. The retinal endothelium releases many dilator (nitric oxide and prostacyclin) and constrictor (endothelin-1, other prostanoids) agents. These vasoactive agents act on the underlying pericytes to regulate local blood flow. A fine balance exists between these agents, which is generally tilted towards the vasodilators. For example, a reduction in the level of nitric oxide or an increase in ET-1 could result in vasospasm. Impaired nitric oxide production has been implicated in systemic vascular diseases. Also, elevated levels of ET-1 have been implicated in NTG.
Endothelial cells lining the retinal microvascular system are exposed to shear stress and cyclic strain. Chronic changes in these mechanical forces lead to alterations in production of the vasoactive agents described. Consequently, we are investigating the responsiveness of retinal endothelial and pericyte cells to these hemodynamic stimuli.
