Environmental and cortisol-mediated control of Ca 2+ uptake in tilapia ( Oreochromis mossambicus )

Ca 2+ is a vital element for many physiological processes in vertebrates, including teleosts, which live in aquatic environments and acquire Ca 2+ from their surroundings. Ionocytes within the adult gills or larval skin are critical sites for transcellular Ca 2+ uptake in teleosts. The ionocytes of zebrafish were found to contain transcellular Ca 2+ transporters, epithelial Ca 2+ channel (ECaC), plasma membrane Ca 2+ -ATPase 2 (PMCA2), and Na + /Ca 2+ exchanger 1b (NCX1b), providing information about the molecular mechanism of transcellular Ca 2+ transports mediated by ionocytes in fish. However, more evidence is required to establish whether or not a similar mechanism of transcellular Ca 2+ 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 Ca 2+ transport through ionocytes previously proposed for zebrafish. In addition, we also reveal that low Ca 2+ water treatment of tilapia stimulates Ca 2+ 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 Ca 2+ influx and ecac expression. Therefore, increased cyp11b expression is suggested to enhance Ca 2+ uptake capacity in tilapia exposed to low Ca 2+ water. Furthermore, the application of cortisol receptor antagonists revealed that cortisol may regulate Ca 2+ 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.