Basigin gene products associate to form a novel cell‐adhesion system used to maintain a metabolic cytoarchitecture and potentially stimulate an immune response in the neural retina

Abstract

Two Basigin gene products are expressed in the vertebrate neural retina, named Basigin‐variant‐ 1 and Basigin‐variant‐2. Variant‐2 is found on cells throughout the body, including monocytes, as well as on the surface of Muller glial cells and retinal pigmented epithelial cells of the mammalian eye, whereas variant‐1 is considered a photoreceptor‐specific gene product. These membrane‐associated glycoproteins, which are members of the immunoglobulin (Ig) superfamily, are identical in amino acid sequence except for an additional Ig domain at the amino terminus of Basigin‐variant‐1. The amino acid sequence of the Basigin‐variant‐1‐specific Ig domain is well conserved throughout evolution, which suggests that it performs a conserved function. In addition, the Basigin‐variant‐1‐specific Ig domain is similar in amino acid sequence to a region of L1cam, a known Basigin‐variant‐2 binding partner in the brain. Therefore, the purpose of this study was to test the hypothesis that the Basigin‐variant‐1‐specific Ig domain binds to Basigin‐variant‐2. Recombinant forms of the Basigin‐variant‐1‐specific Ig domain and L1cam were generated via molecular techniques and used in enzyme‐linked immunosorbent assay (ELISA) binding assays with Basigin‐variant‐2 endogenously expressed in mouse neural retina and kidney, as well as the mouse monocytic cell line RAW 264.7. The results of the study indicate that the Basigin‐variant‐1‐specific Ig domain does bind Basigin‐variant‐2 with moderate affinity. The corresponding region of L1cam, however, does not interact with Basigin‐variant‐2, which suggests that amino acids within this highly conserved domain that are specific to Basigin‐variant‐ 1 but not L1cam are responsible for the interaction. The data suggest that Basigin‐variant‐1 does interact with Basigin‐variant‐2 to form a novel cell adhesion system between Müller cells and photoreceptors in the neural retina. The data also suggest that the same interaction can occur between Basigin‐variant‐1 on photoreceptor cells and Basigin‐variant‐2 on monocytes that invade the neural retina in response to a compromised retinal pigmented epithelium.Support or Funding InformationUNF Office of Academic AffairsThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.