ArticleAmerican journal of physiology. Renal physiology2009
Attenuated, flow-induced ATP release contributes to absence of flow-sensitive, purinergic Cai2+ signaling in human ADPKD cyst epithelial cells.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 81 citations in OpenAlex.
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Pathogenic Pathways and Therapeutic Strategies in Autosomal Dominant Polycystic Kidney Disease (ADPKD).Journal of cellular signaling · 2025Article
- Shear stress effects on epididymal epithelial cell via primary cilia mechanosensory signaling.Journal of cellular physiology · 2025Article
- Functions of cilia in cardiac development and disease.Annals of human genetics · 2024Review
- Involvement of ceramide biosynthesis in increased extracellular vesicle release inFrontiers in endocrinology · 2022Article
- Recent advances in understanding ion transport mechanisms in polycystic kidney disease.Clinical science (London, England : 1979) · 2021Review
- Conversion of extracellular ATP into adenosine: a master switch in renal health and disease.Nature reviews. Nephrology · 2020Review
- Polycystin-1 regulates ARHGAP35-dependent centrosomal RhoA activation and ROCK signaling.JCI insight · 2020Article
- Rapamycin treatment correlates changes in primary cilia expression with cell cycle regulation in epithelial cells.Biochemical pharmacology · 2020Article
- Modulation of polycystic kidney disease by G-protein coupled receptors and cyclic AMP signaling.Cellular signalling · 2020Review
- Sensing of tubular flow and renal electrolyte transport.Nature reviews. Nephrology · 2020Review
- Extracellular Nucleotides and P2 Receptors in Renal Function.Physiological reviews · 2020Review
- Fundamental insights into autosomal dominant polycystic kidney disease from human-based cell models.Pediatric nephrology (Berlin, Germany) · 2019Article
- Characterization of purinergic receptor expression in ARPKD cystic epithelia.Purinergic signalling · 2018Article
- Deficient transient receptor potential vanilloid type 4 function contributes to compromised [CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Cdc42 activation couples fluid shear stress to apical endocytosis in proximal tubule cells.Physiological reports · 2017Article
- The mechanosensitive BKα/β1 channel localizes to cilia of principal cells in rabbit cortical collecting duct (CCD).American journal of physiology. Renal physiology · 2017Article
- P2Y2R is a direct target of HIF-1α and mediates secretion-dependent cyst growth of renal cyst-forming epithelial cells.Purinergic signalling · 2016Article
- Transcriptome analysis reveals manifold mechanisms of cyst development in ADPKD.Human genomics · 2016Article
- Calcium channels in primary cilia.Current opinion in nephrology and hypertension · 2016Review
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9 authors at 3 institutions in 1 country.
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Abstract
Flow-induced cytosolic Ca2+ Ca(i)2+ signaling in renal tubular epithelial cells is mediated in part through P2 receptor (P2R) activation by locally released ATP. The ability of P2R to regulate salt and water reabsorption has suggested a possible contribution of ATP release and paracrine P2R activation to cystogenesis and/or enlargement in autosomal dominant polycystic kidney disease (ADPKD). We and others have demonstrated in human ADPKD cyst cells the absence of flow-induced Ca(i)2+ signaling exhibited by normal renal epithelial cells. We now extend these findings to primary and telomerase-immortalized normal and ADPKD epithelial cells of different genotype and of both proximal and distal origins. Flow-induced elevation of Ca(i)2+ concentration ([Ca2+](i)) was absent from ADPKD cyst cells, but in normal cells was mediated by flow-sensitive ATP release and paracrine P2R activation, modulated by ecto-nucleotidase activity, and abrogated by P2R inhibition or extracellular ATP hydrolysis. In contrast to the elevated ATP release from ADPKD cells in static isotonic conditions or in hypotonic conditions, flow-induced ATP release from cyst cells was lower than from normal cells. Extracellular ATP rapidly reduced thapsigargin-elevated [Ca2+](i) in both ADPKD cyst and normal cells, but cyst cells lacked the subsequent, slow, oxidized ATP-sensitive [Ca2+](i) recovery present in normal cells. Telomerase-immortalized cyst cells also exhibited altered CD39 and P2X7 mRNA levels. Thus the loss of flow-induced, P2R-mediated Ca(i)2+ signaling in human ADPKD cyst epithelial cells was accompanied by reduced flow-sensitive ATP release, altered purinergic regulation of store-operated Ca2+ entry, and altered expression of gene products controlling extracellular nucleotide signaling.
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