Abstract
Defects in the glycocalyx of the bladder epithelium may be related to the opment of bladder diseases including interstitial cystitis which is a chronic bladder e of unknown etiology. Indirect evidence has implicated alterations in the bladder elial glycoconjugates in interstitial cystitis and vesicaler instillation of aminoglycans is promoted as treatments. However, information on the nature of the onjugates of the bladder epithelium and lectins that may interact with the exogenous ed glycoconjugates is very limited. We have examined the endogenous lectin ated with bladder epithelium by immunohistochemistry using biotinylated ycoconjugates. The strong calcium-independent binding of β-D-galactose probe sted the presence of galectins in rabbit and human bladder. Extracts of rabbit er organ cultures metabolically labeled with [14cJ-amino acids were subjected to y chromatography on immobilized lactose and the specifically bound material eluted 0.2 M lactose. SDS-PAGE of the recovered proteins revealed a major band of ximately 30 kDa and a minor band of 21 kDa. Polymerase chain reaction and rn blot analysis showed that both galectin-3 and galectin-4 are expressed in rabbit r. Since galectin-3 from rabbit had been previously cloned, we cloned and ced galectin-4 from rabbit bladder. The deduced full length sequence of 328 amino evealed four distinct regions; a N-terminal peptide of 19 residues, two carbohydrate recognition domains of 130 residues each, and a linker region of 49 residues. Comparison of the rabbit galectin-4 sequence with those of human, pig, rat, and mouse revealed two invariant peptide motifs that are proposed as signature sequences for identifying related galectins. recognition domains of 130 residues each, and a linker region of 49 residues. Comparison
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Bhavanandan, V.P., Puch, S., Guo, X., Jiang, W. (2001). Galectins and Other Endogenous Carbohydrate-Binding Proteins of Animal Bladder. In: Wu, A.M. (eds) The Molecular Immunology of Complex Carbohydrates —2. Advances in Experimental Medicine and Biology, vol 491. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1267-7_7
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DOI: https://doi.org/10.1007/978-1-4615-1267-7_7
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