Irvine, Calif., July 30, 2013 — By understanding how water flows in and out of eye lens cells, UC Irvine and Howard Hughes Medical Institute researchers are providing new insights into the underlying molecular mechanisms that can lead to cataracts.
James Hall, professor of physiology & biophysics, and colleagues identified how two proteins – aquaporin zero and calmodulin – interact to throw a molecular switch that controls the flow of water through the cell membrane, working much like a gate valve in a plumbing fixture.
Proper hydration of the membrane helps assure good cell health, and any disruption in this flow or its regulation results in cataract formation.
“We know that defects in aquaporin zero lead to congenital cataracts. Our study makes a step toward understanding how cataracts form and, we hope, learning how to prevent or delay them,” said Hall. He teamed with HHMI’s Tamir Gonen to lead the study, which appears online in Nature Structural & Molecular Biology.
A cataract is a clouding of the lens inside the eye which decreases vision and, unless treated, is the most common cause of blindness. Although cataract surgery is widely available in the U.S. and other developed countries, a majority of the world’s population does not have access to this procedure, Hall added, and, even in developed countries, delaying the average age of cataract onset would dramatically reduce healthcare costs.
Daniel Clemens, J. Alfredo Freites, Karin Nemeth-Cahalan, Matthias Heyden and Douglas Tobias of UC Irvine; and Steve Reichow of HHMI contributed to the study, which received support from the HHMI and the National Eye Institute (grant EY5661).