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

Galectin 3 belongs to a family of glycoconjugate-binding proteinsthat participate in cellular homeostasis by modulating cellgrowth, adhesion, and signaling. We studied adult galectin 3null mutant (Gal 3–/–) and wild-type (WT) mice togain insights into the role of galectin 3 in the kidney. Byimmunofluorescence, galectin 3 was found in collecting duct(CD) principal and intercalated cells in some regions of thekidney, as well as in the thick ascending limbs at lower levels.Compared to WT mice, Gal 3–/– mice had ~11% fewerglomeruli (p < 0.04), associated with kidney hypertrophy(p < 0.006). In clearance experiments, urinary chloride excretionwas found to be higher in Gal 3–/– than in WT mice(p < 0.04), but there was no difference in urinary bicarbonateexcretion, in glomerular filtration, or urinary flow rates.Under chronic low sodium diet, Gal 3–/– mice hadlower 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 observedincrease in -epithelial sodium channel (-ENaC) protein abundancein the mutant mice (p < 0.001). Chronic high sodium dietresulted 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 ECFvolume contraction and reduced blood pressure levels.