(405) 271-8001 Ext. 46478
Education:
PhD, Anatomy and Cell Biology, University of North Dakota, School of Medicine, Grand Forks, North Dakota
BS, Cytotechnology, University of North Dakota, School of Medicine, Grand Forks, North Dakota
Clinical/Research Interests:
Myopia (“nearsightedness”) is a significant global public health concern. The incidence of myopia is reaching epidemic proportions, as have the serious ocular complications associated with high myopia. It is well established that postnatal eye growth is controlled via a cascade of locally generated chemical events that are initiated in the retina and ultimately cause changes in scleral extracellular matrix (ECM) remodeling to effect changes in eye size and refraction. Therefore our long-term goal is to identify the effector molecules that mediate scleral remodeling as they may facilitate the design of therapies to slow or prevent the progression of myopia. Data is accumulating to suggest that all-trans-retinoic acid (atRA) is an important molecular signal for the control of postnatal ocular growth. We have recently demonstrated that in response to visual stimuli, ocular atRA synthesis is regulated exclusively via choroidal expression of retinaldehyde dehydrogenase 2 (RALDH2). Furthermore, we have compelling evidence to suggest that apolipoprotein A-1 (ApoA-1) functions as a specific extracellular atRA-binding protein in the choroid and participates in a regulatory feedback mechanism with atRA for the regulation of atRA transport and activity on ocular targets. Therefore, the objective of our current research is to define the key events that regulate choroidal atRA synthesis, transport and activity in scleral remodeling during visually guided ocular growth.