After receiving his doctorate at the University of East Anglia in his native country England, Nicholas Delamere brought his work on membrane transport physiology to the University of Colorado, where he spent ten years. He moved to the University of Louisville in 1986 where he established a laboratory to study the mechanisms which control ocular pressure, fluid movement and the regulation of ion transport molecules in lens and optic nerve. In 2006, together with several lab members, he joined the University of Arizona. In essence, Dr. Delamere examines the manner in which cells transport salt and water. Too much fluid (aqueous humor) secreted into the eye can increase pressure within the eye, leading to glaucoma and retinal damage. Dr. Delamere's research team seeks to regulate these transport mechanisms on the molecular level, with the eventual goal of developing drugs to maintain this intraocular balance and reduce the incidence of glaucoma. In another area of research, Dr. Delamere tackles the problem of age-related cataracts and how they can be affected by regulating the activity of the membrane transport pump Na,K-ATPase. Since human lenses contain the same cells from conception to death, with no tissue regeneration or loss, this area of research offers a promising model for tissue preservation, anti-aging constructs and neuroprotection in the brain. Reducing the onset of cataracts through membrane transport physiology, even for a few more years, would result in huge savings of cost, effort and anxiety.
Nicholas A Delamere, PhD
- Professor, Physiology
- Professor, Ophthalmology
- Professor, BIO5 Institute
- Member of the Graduate Faculty
Shahidullah M, Mandal A, Delamere NA. "Activation of TRPV1 channels leads to stimulation of NKCC1 cotransport in the lens." Am. J. Physiol., Cell Physiol.. 2018. PMID: 30207782
Matagne V, Wondolowski J, Frerking M, et al. "Correcting deregulated Fxyd1 expression rescues deficits in neuronal arborization and potassium homeostasis in MeCP2 deficient male mice." Brain Res.. 2018;1697:45-52. PMID: 29902467