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Relations between intracellular Ca 2+ stores and store‐operated Ca 2+ entry in primary cultured human glioblastoma cells
Author(s) -
Hartmann Jana,
Verkhratsky Alexej
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.411bb.x
Subject(s) - extracellular , intracellular , endoplasmic reticulum , purinergic receptor , mitochondrion , biophysics , inositol , calcium , microbiology and biotechnology , chemistry , fura 2 , biochemistry , biology , cytosol , receptor , enzyme , organic chemistry
1 In primary cultured human glioblastoma cells extracellular application of ATP triggered elevation in cytoplasmic calcium concentration ([Ca 2+ ] i ) mediated entirely by generation of inositol 1,4,5‐trisphosphate (Ins P 3 )‐dependent Ca 2+ release from endoplasmic reticulum Ca 2+ stores followed by the activation of store‐operated Ca 2+ entry into the cells. 2 Sensitivity of P 2Y purinoceptors to extracellular ATP was regulated by extracellular Ca 2+ : in Ca 2+ ‐free extracellular solution the threshold concentration of ATP that induced an increase in [Ca 2+ ] i was reduced by one order of magnitude. 3 Activation of Ca 2+ release and store‐operated Ca 2+ entry was dissociated: low concentrations of ATP induced substantial Ca 2+ release without activation of Ca 2+ entry; activation of the latter required higher ATP concentrations. 4 Mitochondria participated in buffering Ca 2+ loads that resulted from store‐operated Ca 2+ influx; in contrast Ca 2+ released from intracellular stores was not accumulated by the mitochondrial depot. 5 We conclude that ATP‐induced Ca 2+ responses are governed by several pathways with different sensitivities to the agonist. This enables cells to respond either with pure Ca 2+ release from intracellular stores (at low ATP concentrations) or (at high ATP concentrations) the response is amplified by plasmalemmal Ca 2+ influx. Store‐operated Ca 2+ entry increases mitochondrial Ca 2+ content providing a link between cellular activation and mitochondrial function.