Two papers to be published in the Early Edition online of the Proceedings of the National Academy of Sciences (PNAS) the week of July 30-August 3, 2007 report findings that demonstrate that neuroprotectin D1 (NPD1) protects against damage to retinal pigment epithelial (RPE) cells and identifies an important trigger for its production and novel molecular mechanisms that support vision. The research was conducted at LSU Health Sciences Center New Orleans and the papers are entitled Neurotrophins enhance retinal pigment epithelial cell survival through neuroprotectin D1 signaling and Photoreceptor outer segment phagocytosis attenuates oxidative stress-induced apoptosis with concomitant neuroprotectin D1 synthesis. RPE cells are responsible for the renewal of the tips of photoreceptor cells (rods and cones) crucial to vision.
Neuroprotectin D1 is a messenger (mediator) discovered by Nicolas Bazan, MD, PhD, Boyd Professor, Ernest C. and Yvette C. Villere Professor of Ophthalmology, and Director of the Neuroscience Center of Excellence at LSU Health Sciences Center New Orleans, and his colleagues that represents one of the most powerful endogenous (made by the body) neuroprotective mediators known. Its precursor is DHA (docosahexaenoic acid), an essential fatty acid (must be provided by the diet) of the omega-3 fatty acid family enriched in RPE cells in the retina and brain. DHA is a target of oxidative stress in pathological conditions and Dr. Bazans research recently showed that RPE cells create NPD1 in response to oxidative stress.
The LSUHSC scientists discovered that neurotrophins (small proteins critical in cell survival and death) trigger NPD1 synthesis. They demonstrate that the endogenous toxic component (A2E) that accumulates in the retina during aging and in retinal degenerations, including those due to gene mutations, can be counteracted by NPD1.
The LSUHSC research team conducted studies on the formation and action of NPD1 on a human tra
Contact: Leslie Capo
Louisiana State University Health Science Center