The present study was conducted on human Jurkat T-cell lines in order to elucidate the role of phospholipase A 2 in capacitative calcium entry. We have employed thapsigargin (TG) that induces increases in [Ca 2+ ] i by emptying the calcium pool of endoplasmic reticulum, followed by capacitative calcium entry. We designed a Ca 2+ free/Ca 2+ reintroduction (CFCR) protocol for the experiments, conducted in Ca 2+ -free medium. By employing CFCR protocol, we observed that addition of exogenous arachidonic acid (AA) stimulated TG-induced capacitative calcium influx. The liberation of endogenous AA and its autocrine action seems to be implicated during TGinduced capacitative calcium influx: TG potentiates the induction of constitutively expressed mRNA of four PLA 2 isoforms (type 1B, IV, V, VI), the inhibitors of the three PLA 2 isotypes (type 1B, V, VI) inhibit TG-induced release of [ 3 H]AA into the extracellular medium, and finally, these PLA 2 inhibitors do curtail TG-stimulated capacitative calcium entry in these cells. These results suggest that stimulation of three isoforms of PLA 2 by thapsigargin liberates free AA that, in turn, induces capacitative calcium influx in human T-cells.
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