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(American Journal of Pathology. 2006;169:1925-1938.)
© 2006 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2006.060245

Galectin-3 Associates with the Primary Cilium and Modulates Cyst Growth in Congenital Polycystic Kidney Disease

Miliyun G. Chiu*, Tanya M. Johnson*, Adrian S. Woolf*, Eugenia M. Dahm-Vicker*, David A. Long*, Lisa Guay-Woodford{dagger}, Katherine A. Hillman*, Suleman Bawumia{ddagger}, Kerrie Venner§, R. Colin Hughes{ddagger}, Francoise Poirier and Paul J.D. Winyard*

From the Nephro-Urology Unit,* Institute of Child Health, and the Electron Microscopy Unit, Institute of Neurology,§ University College London, London, United Kingdom; the National Institute for Medical Research,{ddagger} London United Kingdom; the Department of Developmental Biology, Institut Jacques Monod, Paris, France; and the University of Alabama at Birmingham,{dagger} Birmingham, Alabama

Several lines of evidence implicate the ß-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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