Exploring the role of galectin 3 in kidney function: a genetic approach

Galectin 3 belongs to a family of glycoconjugate-binding proteins that participate in cellular homeostasis by modulating cell growth, adhesion, and signaling. We studied adult galectin 3 null mutant ( Gal 3(-/-))and wild-type (WT) mice to gain insights into the role of galectin 3 in the kidney. By immunofluorescence, galectin 3 was found in collecting duct ( CD) principal and intercalated cells in some regions of the kidney, as well as in the thick ascending limbs at lower levels. Compared to WT mice, Gal 3(-/-) mice had similar to 11% fewer glomeruli ( p < 0.04), associated with kidney hypertrophy ( p < 0.006). In clearance experiments, urinary chloride excretion was found to be higher in Gal 3(-/-) than in WT mice ( p < 0.04), but there was no difference in urinary bicarbonate excretion, in glomerular filtration, or urinary flow rates. Under chronic low sodium diet, Gal 3(-/-) mice had lower extracellular fluid (ECF) volume than WT mice ( p < 0.05). Plasma aldosterone concentration was higher in Gal 3(-/-) than in WT mice ( p < 0.04), which probably caused the observed increase in alpha-epithelial sodium channel (alpha-ENaC) protein abundance in the mutant mice ( p < 0.001). Chronic high sodium diet resulted paradoxically in lower blood pressure ( p < 0.01) in Gal 3(-/-) than in WT. We conclude that Gal 3(-/-) mice have mild renal chloride loss, which causes chronic ECF volume contraction and reduced blood pressure levels.