Background: Freshwater fish absorb Ca 2+ predominantly from ambient water, and more than 97% of Ca 2+ uptake is achieved by active transport through gill mitochondrion-rich (MR) cells. In the current model for Ca 2+ uptake in gill MR cells, Ca 2+ passively enters the cytosol via the epithelium Ca 2+ channel (ECaC), and then is extruded into the plasma through the basolateral Na + / Ca 2+ exchanger (NCX) and plasma membrane Ca 2+ -ATPase (PMCA). However, no convincing molecular or cellular evidence has been available to support the role of specific PMCA and/or NCX isoforms in this model. Zebrafish (Danio rerio) is a good model for analyzing isoforms of a gene because of the plentiful genomic databases and expression sequence tag (EST) data.

Ca2+ is a vital element for many physiological processes in vertebrates, including teleosts, which live in aquatic environments and acquire Ca2+ from their surroundings. Ionocytes within the adult gills or larval skin are critical sites for transcellular Ca2+ uptake in teleosts. The ionocytes of zebrafish were found to contain transcellular Ca2+ transporters, epithelial Ca2+ channel (ECaC), plasma membrane Ca2+-ATPase 2 (PMCA2), and Na+/Ca2+ exchanger 1b (NCX1b), providing information about the molecular mechanism of transcellular Ca2+ transports mediated by ionocytes in fish. However, more evidence is required to establish whether or not a similar mechanism of transcellular Ca2+ transport also exists in others teleosts. In the present study, ecac, pmca2, and ncx1 were found to be expressed in the branchial ionocytes of tilapia, thereby providing further support for the mechanism of transcellular Ca2+ transport through ionocytes previously proposed for zebrafish. In addition, we also reveal that low Ca2+ water treatment of tilapia stimulates Ca2+ uptake and expression of ecac and cyp11b (the latter encodes a cortisol-synthesis enzyme). Treatment of tilapia with exogenous cortisol (20 mg/l) enhanced both Ca2+ influx and ecac expression. Therefore, increased cyp11b expression is suggested to enhance Ca2+ uptake capacity in tilapia exposed to low Ca2+ water. Furthermore, the application of cortisol receptor antagonists revealed that cortisol may regulate Ca2+ uptake through glucocorticoid and/or mineralocorticoid receptor (GR and/or MR) in tilapia. Taken together, the data suggest that cortisol may activate GR and/or MR to execute its hypercalcemic action by stimulating ecac expression in tilapia.

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