Associate Professor Donaldson directs the The Molecular Vision Laboratory. The MVL has extensive molecular and cellular expertise in the general field of membrane transport. Members of the laboratory utilize electrophysiology, imaging, biochemistry, proteomics, molecular biology, and computer modeling to determine how the properties of ion channels and transporters contribute to the integrative function of ocular tissues that comprise the front of the eye. Research projects in the lens are focused on determining how the interaction of a variety of ion channels and transporters contribute to the maintenance of lens transparency. It has been proposed that spatial differences in ion channels and transporters drive an internal microcirculation system, which in the absence of a blood supply delivers nutrients and controls the volume of the lens. We have hypothesized that a decline in the ability to deliver nutrients, including the antioxidants that protect the lens against oxidative damage, is an initiator of old age cataract, the leading cause of blindness in the world today. By mapping the antioxidant pathways in different regions of the lens we hope to be able to identify strategies that will enhance antioxidant delivery and thereby delay the onset of cataract. Diabetic cataract is associated with a loss of cell volume in cortical lens cells. Other projects in the MVL are investigating the cellular mechanisms responsible for the maintenance of lens volume. Here the emphasis is to characterize the mechanisms involved with the view to identify drug targets against which anti-cataract therapies can be designed.
While the majority of projects currently involve the lens, work on the ciliary body has focused the gap junctions that functionally couple the two distinctly different cell layers that comprise the ciliary epithelium. These cell-to-cell channels are thought represent a rate limiting step in the secretion of the aqueous humour. Hence they represent a potential target for the development of anti-glaucoma therapies designed to lower intraocular pressure via reducing the production of aqueous humor. Similary, work on the cornea has concentrated on determining the role played by gap junction channels in the differentiation and maintenance of the corneal epithelium. Here our hypothesis is that modulation of connexin expression can influence the response of the cornea to wound healing. Thus research in the MVL strives to advance our understanding of the cellular and molecular mechanisms underlying ocular diseases associated with the front of the eye
