Galectin-3 modulates ureteric bud branching in organ culture of the developing mouse kidney

Galectin-3 is a mammalian beta -galactoside-specific lectin with functions in cell growth, adhesion, and neoplastic transformation. On the basis of ex pression patterns in humans, it is proposed that galectin-3 modulates fetal collecting duct growth. This article provides evidence that galectin3 can modulate branching morphogenesis of the mouse ureteric bud/ collecting duct lineage. With the use of immunohistochemistry, galectin-3 was not detected in early metanephrogenesis but was upregulated later in fetal kidney matur ation when the protein was prominent in basal domains of medullary collecti ng ducts. Addition of galectin-3 to embryonic days 11 and 12 whole metaneph ric cultures inhibited ureteric bud branching, whereas galectin-1 did not p erturb morphogenesis, nor did a galectin-3 mutant lacking wild-type high-af finity binding to extended oligosaccharides. Exogenous galectin-3 retarded conversion of renal mesenchyme to nephrons in whole metanephric explants bu t did not affect nephron induction by spinal cord in isolated renal mesench ymes. Finally, addition of a blocking antiserum to galectin-3 caused dilati on and distortion of developing epithelia in embryonic day 12 metanephroi c ultured for 1 wk. The upregulation of galectin-3 protein during kidney matu ration, predominantly at sites where it could mediate cell/matrix interacti ons, seems to modulate growth of the ureteric tree.