ArticleBMC nephrology2013
Intracellular calcium release modulates polycystin-2 trafficking.
Article in BMC nephrology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Role of PKD2 in the endoplasmic reticulum calcium homeostasis.Frontiers in physiology · 2022Review
- Polycystin-2 Is Required for Chondrocyte Mechanotransduction and Traffics to the Primary Cilium in Response to Mechanical Stimulation.International journal of molecular sciences · 2021Article
- Activation of Calcium-Sensing Receptor increases intracellular calcium and decreases cAMP and mTOR in PKD1 deficient cells.Scientific reports · 2018Article
- Polycystin and calcium signaling in cell death and survival.Cell calcium · 2018Review
- Activation of the Calcium-Sensing Receptor Corrects the Impaired Mitochondrial Energy Status Observed in Renal Polycystin-1 Knockdown Cells Modeling Autosomal Dominant Polycystic Kidney Disease.Frontiers in molecular biosciences · 2018Article
- A polycystin-centric view of cyst formation and disease: the polycystins revisited.Kidney international · 2015Review
- Article
- Channelopathies.Korean journal of pediatrics · 2014Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPolycystin-2 (PC2), encoded by the gene that is mutated in autosomal dominant polycystic kidney disease (ADPKD), functions as a calcium (Ca(2+)) permeable ion channel. Considerable controversy remains regarding the subcellular localization and signaling function of PC2 in kidney cells.
methodsWe investigated the subcellular PC2 localization by immunocytochemistry and confocal microscopy in primary cultures of human and rat proximal tubule cells after stimulating cytosolic Ca(2+) signaling. Plasma membrane (PM) Ca(2+) permeability was evaluated by Fura-2 manganese quenching using time-lapse fluorescence microscopy.
resultsWe demonstrated that PC2 exhibits a dynamic subcellular localization pattern. In unstimulated human or rat proximal tubule cells, PC2 exhibited a cytosolic/reticular distribution. Treatments with agents that in various ways affect the Ca(2+) signaling machinery, those being ATP, bradykinin, ionomycin, CPA or thapsigargin, resulted in increased PC2 immunostaining in the PM. Exposing cells to the steroid hormone ouabain, known to trigger Ca(2+) oscillations in kidney cells, caused increased PC2 in the PM and increased PM Ca(2+) permeability. Intracellular Ca(2+) buffering with BAPTA, inositol 1,4,5-trisphosphate receptor (InsP3R) inhibition with 2-aminoethoxydiphenyl borate (2-APB) or Ca(2+)/Calmodulin-dependent kinase inhibition with KN-93 completely abolished ouabain-stimulated PC2 translocation to the PM.
conclusionsThese novel findings demonstrate intracellular Ca(2+)-dependent PC2 trafficking in human and rat kidney cells, which may provide new insight into cyst formations in ADPKD.
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