Retinal Degeneration Following Failed Photoreceptor Maturation in 5A11/Basigin Null Mice

Abstract

5A11/Basigin is a member of the immunoglobulin gene superfamily which plays an important role in cell–cell interactions in the developing neural retina. These studies were initiated to investigate the distribution of 5A11/Basigin within the mouse retina, as well as the cytoarchitectural and biochemical effects on the retina after the inactivation of the 5A11/Basigin gene in a mouse strain. Immunocytochemical analyses indicated that mouse 5A11/Basigin is located on the surface of Müller cells, the apical and basal surfaces of the retinal pigmented epithelium, and blood vessels. Lower expression levels were found on photoreceptor cell bodies and a portion of the inner segments. Inactivation of the 5A11/Basigin gene in mice resulted in the failure of photoreceptor cells to fully mature. This failed development eventually lead to the degeneration, death and removal of most of the photoreceptors several months after birth. Biochemical analyses indicated that expression of Müller cell specific proteins, including glutamine synthetase and carbonic anhydrase-II, was not effected; however, opsin protein expression never achieved normal adult levels in the 5A11/Basigin null mice. Also, 5A11/Basigin null retinas were considered ‘reactive’ based on elevated glial fibrillary acidic protein expression. The results presented here suggest that 5A11/Basigin expression on Müller cells and/or the retinal pigmented epithelium is necessary for photoreceptor outer segment biochemical development and structural maintenance. However, the exact role that 5A11/Basigin plays during retinal development remains to be determined.