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• W2082518476 abstract "Renal epithelial cells release ATP constitutively under basal conditions and release higher quantities of purine nucleotide in response to stimuli. ATP filtered at the glomerulus, secreted by epithelial cells along the nephron, and released serosally by macula densa cells for feedback signaling to afferent arterioles within the glomerulus has important physiological signaling roles within kidneys. In autosomal recessive polycystic kidney disease (ARPKD) mice and humans, collecting duct epithelial cells lack an apical central cilium or express dysfunctional proteins within that monocilium. Collecting duct principal cells derived from an Oak Ridge polycystic kidney (orpk ( Tg737 ) ) mouse model of ARPKD lack a well-formed apical central cilium, thought to be a sensory organelle. We compared these cells grown as polarized cell monolayers on permeable supports to the same cells where the apical monocilium was genetically rescued with the wild-type Tg737 gene that encodes Polaris, a protein essential to cilia formation. Constitutive ATP release under basal conditions was low and not different in mutant versus rescued monolayers. However, genetically rescued principal cell monolayers released ATP three- to fivefold more robustly in response to ionomycin. Principal cell monolayers with fully formed apical monocilia responded three- to fivefold greater to hypotonicity than mutant monolayers lacking monocilia. In support of the idea that monocilia are sensory organelles, intentionally harsh pipetting of medium directly onto the center of the monolayer induced ATP release in genetically rescued monolayers that possessed apical monocilia. Mechanical stimulation was much less effective, however, on mutant orpk collecting duct principal cell monolayers that lacked apical central monocilia. Our data also show that an increase in cytosolic free Ca(2+) primes the ATP pool that is released in response to mechanical stimuli. It also appears that hypotonic cell swelling and mechanical pipetting stimuli trigger release of a common ATP pool. Cilium-competent monolayers responded to flow with an increase in cell Ca(2+) derived from both extracellular and intracellular stores. This flow-induced Ca(2+) signal was less robust in cilium-deficient monolayers. Flow-induced Ca(2+) signals in both preparations were attenuated by extracellular gadolinium and by extracellular apyrase, an ATPase/ADPase. Taken together, these data suggest that apical monocilia are sensory organelles and that their presence in the apical membrane facilitates the formation of a mature ATP secretion apparatus responsive to chemical, osmotic, and mechanical stimuli. The cilium and autocrine ATP signaling appear to work in concert to control cell Ca(2+). Loss of a cilium-dedicated autocrine purinergic signaling system may be a critical underlying etiology for ARPKD and may lead to disinhibition and/or upregulation of multiple sodium (Na(+)) absorptive mechanisms and a resultant severe hypertensive phenotype in ARPKD and, possibly, other diseases." @default.
• W2082518476 created "2016-06-24" @default.
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• W2082518476 date "2007-11-13" @default.
• W2082518476 modified "2023-10-15" @default.
• W2082518476 title "Loss of apical monocilia on collecting duct principal cells impairs ATP secretion across the apical cell surface and ATP-dependent and flow-induced calcium signals" @default.
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• W2082518476 cites W1531796828 @default.
• W2082518476 cites W1680485768 @default.
• W2082518476 cites W1976999827 @default.
• W2082518476 cites W1981196442 @default.
• W2082518476 cites W1984826335 @default.
• W2082518476 cites W1984953412 @default.
• W2082518476 cites W2008602135 @default.
• W2082518476 cites W2010327392 @default.
• W2082518476 cites W2013681980 @default.
• W2082518476 cites W2021709361 @default.
• W2082518476 cites W2027226283 @default.
• W2082518476 cites W2028607959 @default.
• W2082518476 cites W2029085436 @default.
• W2082518476 cites W2033243150 @default.
• W2082518476 cites W2039606438 @default.
• W2082518476 cites W2047345137 @default.
• W2082518476 cites W2047462949 @default.
• W2082518476 cites W2055866154 @default.
• W2082518476 cites W2057772772 @default.
• W2082518476 cites W2061060689 @default.
• W2082518476 cites W2064090272 @default.
• W2082518476 cites W2075591864 @default.
• W2082518476 cites W2086011059 @default.
• W2082518476 cites W2086937811 @default.
• W2082518476 cites W2087887284 @default.
• W2082518476 cites W2095869636 @default.
• W2082518476 cites W2096675347 @default.
• W2082518476 cites W2098360584 @default.
• W2082518476 cites W2098759244 @default.
• W2082518476 cites W2104846745 @default.
• W2082518476 cites W2105622994 @default.
• W2082518476 cites W2106697346 @default.
• W2082518476 cites W2111432014 @default.
• W2082518476 cites W2112200758 @default.
• W2082518476 cites W2119022046 @default.
• W2082518476 cites W2131163999 @default.
• W2082518476 cites W2131427311 @default.
• W2082518476 cites W2133817119 @default.
• W2082518476 cites W2136800297 @default.
• W2082518476 cites W2137043350 @default.
• W2082518476 cites W2144273979 @default.
• W2082518476 cites W2148037731 @default.
• W2082518476 cites W2148640061 @default.
• W2082518476 cites W2154489315 @default.
• W2082518476 cites W2155494705 @default.
• W2082518476 cites W2159467374 @default.
• W2082518476 cites W2161440135 @default.
• W2082518476 cites W2163667338 @default.
• W2082518476 cites W2164020057 @default.
• W2082518476 cites W2164522021 @default.
• W2082518476 cites W2167833375 @default.
• W2082518476 cites W2172276513 @default.
• W2082518476 cites W2182749815 @default.
• W2082518476 cites W2189467740 @default.
• W2082518476 cites W2256588359 @default.
• W2082518476 cites W2271816486 @default.
• W2082518476 cites W2308052730 @default.
• W2082518476 cites W2311800445 @default.
• W2082518476 cites W2314626866 @default.
• W2082518476 cites W2317585161 @default.
• W2082518476 cites W2323803380 @default.
• W2082518476 cites W2345434938 @default.
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• W2082518476 doi "https://doi.org/10.1007/s11302-007-9072-0" @default.
• W2082518476 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2377318" @default.
• W2082518476 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18368523" @default.
• W2082518476 hasPublicationYear "2007" @default.
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