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• W2155494705 abstract "Recent genetic analysis has identified a pivotal role of primary cilia in the pathogenesis of polycystic kidney disease (PKD). However, little is known regarding how cilia loss/dysfunction contributes to cyst development. In epithelial cells, changes in apical fluid flow induce cilia-mediated Ca 2+ entry via polycystin-2 (PC2), a cation channel. The Oak Ridge Polycystic Kidney ( orpk) mouse contains a mutated Tg737 gene that disrupts expression of polaris, a protein required for ciliogenesis. These studies examine the effect of cilia malformation on Ca 2+ entry in orpk cilia(−) collecting duct principal cells, and in orpk cells in which wild-type Tg737 was reintroduced, orpk cilia(+). [Ca 2+ ] i was monitored in confluent cell monolayers using fluorescence microscopy. Intrinsic apical Ca 2+ entry was measured by Mn 2+ quenching and Ca 2+ depletion/readdition under flow conditions below the threshold for stimulation. We found that unstimulated apical Ca 2+ entry was markedly increased in cilia(−) cells and was sensitive to Gd 3+ , an inhibitor of PC2. Electrophysiological measurements demonstrate increased abundance of an apical channel, consistent with PC2, in cilia(−) cells. Immunofluorescence studies revealed that PC2, normally expressed on and at the base of cilia in orpk cilia(+) cells, was observed throughout the apical membrane in cilia(−) cells. Furthermore, cilia(−) cells displayed elevated subapical Ca 2+ levels measured with the near-membrane Ca 2+ indicator FFP-18. We propose that cilia exert a tonic regulatory influence on apical Ca 2+ entry, and absence of cilia results in loss of spatial organization of PC2, causing unregulated Ca 2+ entry and elevations in subapical [Ca 2+ ], a factor which may contribute to cyst formation." @default.
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• W2155494705 date "2006-06-01" @default.
• W2155494705 modified "2023-10-17" @default.
• W2155494705 title "Loss of primary cilia results in deregulated and unabated apical calcium entry in ARPKD collecting duct cells" @default.
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• W2155494705 doi "https://doi.org/10.1152/ajprenal.00463.2005" @default.
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