Congenital hereditary corneal dystrophy (CHED) is an eye disease that presents at birth. As one of the Congenital Corneal Opacities (CCO), CHED causes the corneal endothelium to become cloudy. Patients with the disease exhibit corneal edema and impaired vision. CHED is one of the disorders that are caused by SLC4A11 mutations. SLC4A11 alterations can lead to defects in corneal endothelial cells. Scientists now have made new discoveries on the SLC4A11 protein, a finding that will extend the understanding of CHED and other diseases associated with the gene. The study, conducted by Mark D. Parker, Evan J. Myers, and Aniko Marshall from The State University of New York: The University at Buffalo, and Michael L. Jennings from University of Arkansas for Medical Sciences, appears in Cell Physiology. Parker began to study SLC4A11 protein and its interactions with other proteins about fifteen years ago. SLC4A11 is expressed in corneal endothelial cells and is identified as a borate transporter, but how it works is unclear. Since SLC4A11 is related to CHED, Harboyan syndrome and some cases of Fuchs' endothelial corneal dystrophy, the protein has attracted a lot of attention. Parker’s team set out to elucidate the roles of SLC4A11 in the eyes and ears, especially its function as a transporter. It’s well known that pH balance is essential for health. Parker’s team discovered that SLC4A11 plays a dual role in corneal cells: it can move acid into or out of a cell according to different situations. So they assumed that the protein helps maintain pH balance in these cells. The loss of functional SLC4A11 may result in pH imbalance, making the cells unable to function correctly. Understanding the transport function of SLC4A11 will lead to a deeper understanding of corneal physiology and corneal diseases like CHED. By the way, Flarebio provides SLC4A11 protein and Recombinant Syp with good quality at competitive price.
