Glycobiology Advance Access published online on September 15, 2005
Glycobiology, doi:10.1093/glycob/cwj035
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1 INSERM U426, Faculté de Médecine Xavier Bichat, 16 rue Henri Huchard, 75870 Paris Cedex 18, France; IFR 2 Claude Bernard, Faculté de Médecine Xavier Bichat, 16 rue Henri Huchard, 75870 Paris Cedex 18, France; Université Paris 7, 2 place Jussieu, 75005 Paris, France
* To whom correspondence should be addressed. 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 WT mice to gain insights into the role of galectin 3 in the kidney. By immunofluorescence, galectin 3 was found in collecting duct 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
Received May 30, 2005
Revised August 31, 2005
Accepted September 1, 2005
Article
Exploring the Role of Galectin 3 in Kidney Function: A Genetic Approach
2 Program in Membrane Biology/Renal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA
3 Service de Néphrologie, Hôpital Xavier Bichat, 46 rue Henri Huchard, 75870 Paris Cedex 18, France; Université Paris 7, 2 place Jussieu, 75005 Paris, France
4 Centre d’Explorations Fonctionnelles Intégrées, IFR 2 Claude Bernard, Faculté de Médecine Xavier Bichat, 16 rue Henri Huchard, 75870 Paris Cedex 18, France
5 Association Claude Bernard : Centre de recherche de génétique et pathologie moléculaire de l’hématopoièse, Faculté de Médecine Xavier Bichat, 16 rue Henri Huchard, 75870 Paris Cedex 18, France
6 Institut Jacques Monod, CNRS UMR 7592, Universités Paris 6 and Paris 7, 2 place Jussieu, 75251-Paris Cedex 05, France
7 INSERM U478, Faculté de Médecine Xavier Bichat, 16 rue Henri Huchard, 75870 Paris Cedex 18, France; IFR 2 Claude Bernard, Faculté de Médecine Xavier Bichat, 16 rue Henri Huchard, 75870 Paris Cedex 18, France; Université Paris 7, 2 place Jussieu, 75005 Paris, France
8 Equipe EA 3102, Service d’Anatomopathologie, Hôpital Robert Debré, 75019 Paris, France
Françoise Poirier, E-mail: poirier{at}ijm.jussieu.fr
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Abstract
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 Na 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
-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.![]()
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