| First Author | Chiu MG | Year | 2006 |
| Journal | Am J Pathol | Volume | 169 |
| Issue | 6 | Pages | 1925-38 |
| PubMed ID | 17148658 | Mgi Jnum | J:116210 |
| Mgi Id | MGI:3693172 | Doi | 10.2353/ajpath.2006.060245 |
| Citation | Chiu MG, et al. (2006) Galectin-3 associates with the primary cilium and modulates cyst growth in congenital polycystic kidney disease. Am J Pathol 169(6):1925-38 |
| abstractText | 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. |
