Abstract
BackgroundPolycystic kidney disease (PKD) is characterized by the development of fluid‐filled cysts in the kidney. However, cardiovascular hypertension and aneurysm represent the most serious life‐threatening complications in PKD patients. We have recently shown that polycystins are localized to the endothelial cilia and function in regulating intracellular calcium and nitric oxide synthesis in response to fluid‐shear stress.Methods and ResultsWe show here that two different PKD endothelial cells, Pkd1 (29%) and Tg737 (32%), are characterized by abnormal cell division (p<0.05, compared to wild type cells). We also observe a significant centrosomal over‐duplication, multipolar spindle formation, nuclear fragmentation and polyploidism leading to chromosome instability and mitotic catastrophe in Pkd1 (16%) and Tg737 (20%). These mitotic abnormalities are associated with the down‐regulation of survivin, an inhibitor of apoptosis and a chromosomal passenger protein involved in mitotic spindle checkpoint and regulation of chromosomal segregation.ConclusionTaken together, our findings provide a novel evidence of the roles for ciliary polycystins in regulating cell division through survivin expression and confirm the proposed involvement of cilia in cell division, parallel to their roles as fluid mechanosensors.
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