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

Autor: Dennis Brown, Maurice Bichara, Michel Peuchmaur, Marie Essig, Laetitia Micheli, Françoise Cluzeaud, Zoubida Karim, Isabelle Eude-Le Parco, Françoise Poirier, Amel Attmane-Elakeb, Martine Muffat-Joly, Nicolette Farman, Jean-Pierre Bonvalet
Rok vydání: 2005
Předmět:
Zdroj: Glycobiology. 16:36-45
ISSN: 1460-2423
0959-6658
DOI: 10.1093/glycob/cwj035
Popis: 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 approximately 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.
Databáze: OpenAIRE