Skip Navigation


Glycobiology Advance Access originally published online on September 15, 2005
Glycobiology 2006 16(1):36-45; doi:10.1093/glycob/cwj035
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
16/1/36    most recent
cwj035v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (7)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Bichara, M.
Right arrow Articles by Farman, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bichara, M.
Right arrow Articles by Farman, N.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

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

Maurice Bichara2,3,4, Amel Attmane-Elakeb2,3,4, Dennis Brown5, Marie Essig6,4, Zoubida Karim2,3,4, Martine Muffat-Joly7, Laetitia Micheli8, Isabelle Eude-Le Parco9, Françoise Cluzeaud3,4,10, Michel Peuchmaur11, Jean-Pierre Bonvalet3,4,10, Françoise Poirier1,9 and Nicolette Farman3,4,10

2 INSERM U426, 16 rue Henri Huchard, 75870 Paris Cedex 18, France; 3 IFR 2 Claude Bernard, 16 rue Henri Huchard, 75870 Paris Cedex 18, France; 4 Université Paris 7, 2 place Jussieu, 75005 Paris, France; 5 Program in Membrane Biology/Renal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114; 6 Service de Néphrologie, Hôpital Xavier Bichat, 46 rue Henri Huchard, 75870 Paris Cedex 18, France; 7 Centre d’Explorations Fonctionnelles Intégrées, IFR 2 Claude Bernard, 16 rue Henri Huchard, 75870 Paris Cedex 18, France; 8 Association Claude Bernard, Centre de recherche de génétique et pathologie moléculaire de l’hématopoièse, 16 rue Henri Huchard, 75870 Paris Cedex 18, France; 9 Institut Jacques Monod, CNRS UMR 7592, Universités Paris 6 and Paris 7, 2 place Jussieu, 75251 Paris Cedex 05, France; 10 INSERM U478, 16 rue Henri Huchard, 75870 Paris Cedex 18, France; and 11 Equipe EA 3102, Service d’Anatomopathologie, Hôpital Robert Debré, 75019 Paris, France

1 To whom correspondence should be addressed; e-mail: poirier{at}ijm.jussieu.fr

Received on May 30, 2005; revised on August 31, 2005; accepted on September 1, 2005

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 ~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.

Key words: blood pressure / body fluid volumes / hyperfiltration / Bartter’s like syndrome / null mutant mouse


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 EndocrinologyHome page
A. Nguyen Dinh Cat, A. Ouvrard-Pascaud, F. Tronche, M. Clemessy, D. Gonzalez-Nunez, N. Farman, and F. Jaisser
Conditional Transgenic Mice for Studying the Role of the Glucocorticoid Receptor in the Renal Collecting Duct
Endocrinology, May 1, 2009; 150(5): 2202 - 2210.
[Abstract] [Full Text] [PDF]

Home page
 GlycobiologyHome page
I. Eude-Le Parco, G. Gendronneau, T. Dang, D. Delacour, V. L Thijssen, W. Edelmann, M. Peuchmaur, and F. Poirier
Genetic assessment of the importance of galectin-3 in cancer initiation, progression, and dissemination in mice
Glycobiology, January 1, 2009; 19(1): 68 - 75.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
A. Di Zhang, A. N. D. Cat, C. Soukaseum, B. Escoubet, A. Cherfa, S. Messaoudi, C. Delcayre, J.-L. Samuel, and F. Jaisser
Cross-Talk Between Mineralocorticoid and Angiotensin II Signaling for Cardiac Remodeling
Hypertension, December 1, 2008; 52(6): 1060 - 1067.
[Abstract] [Full Text] [PDF]

Home page
 J. Cell Sci.Home page
D. Delacour, A. Koch, W. Ackermann, I. E.-L. Parco, H.-P. Elsasser, F. Poirier, and R. Jacob
Loss of galectin-3 impairs membrane polarisation of mouse enterocytes in vivo
J. Cell Sci., February 15, 2008; 121(4): 458 - 465.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
M. G. Chiu, T. M. Johnson, A. S. Woolf, E. M. Dahm-Vicker, D. A. Long, L. Guay-Woodford, K. A. Hillman, S. Bawumia, K. Venner, R. C. Hughes, et al.
Galectin-3 Associates with the Primary Cilium and Modulates Cyst Growth in Congenital Polycystic Kidney Disease
Am. J. Pathol., December 1, 2006; 169(6): 1925 - 1938.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.