References
Query Results -- Details
MGI Accession ID: MGI:3693172
J Number: J:116210
Other Accession IDs:
Title: Galectin-3 associates with the primary cilium and modulates cyst growth in congenital polycystic kidney disease.
Authors: Chiu MG; Johnson TM; Woolf AS; Dahm-Vicker EM; Long DA; Guay-Woodford L; Hillman KA; Bawumia S; Venner K; Hughes RC; Poirier F; Winyard PJ
Journal: Am J Pathol
Volume: 169
Issue: 6
Date: 2006 Dec
Year: 2006
Pages: 1925-38
Review Status: Peer Reviewed
Abstract:
Several lines of evidence implicate the beta-galactoside-binding lectin galectin-3 in development and pathological processes in renal collecting ducts: galectin-3 is expressed in the ureteric bud/collecting duct lineage during nephrogenesis, modulates collecting duct growth/differentiation in vitro, and is expressed in human autosomal recessive polycystic kidney disease in cyst epithelia, almost all of which arise from collecting ducts. Moreover, exogenous galectin-3 restricts growth of cysts generated by Madin-Darby canine kidney collecting duct-derived cells in three-dimensional culture in collagen. Using the cpk mouse model of recessively inherited polycystic kidney disease, we observed widespread galectin-3 mRNA and protein in cyst epithelia. Exogenous galectin-3 reduced cyst formation in suspension culture, and mice-null mutant for galectin-3 had more extensive renal cysts in vivo. Galectin-3 was also detected for the first time in the centrosome/primary cilium, which has been implicated in diverse polycystic kidney disease. Cilia structure/number appeared normal in galectin-3-null mutants. Finally, paclitaxel, a therapy that retards polycystic kidney disease in cpk mice, increased extracellular galectin-3, in which the lectin could potentially interact with cilia. These data raise the possibility that galectin-3 may act as a natural brake on cystogenesis in cpk mice, perhaps via ciliary roles.
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