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The aim of the present study was to investigate the regulation of calcium influx in thyroid FRTL-5 cells. Stimulating Fura 2-loaded cells with thapsigargin rapidly increased the cytosolic Ca2+ concentration ([Ca2+]i), which then stabilized at a new elevated plateau level. The initial increase in [Ca2+]i consisted mainly of the release of sequestered Ca2+. The plateau phase was totally dependent on extracellular Ca2+. The influx of Ca2+ was blocked by Ni2+ and was decreased in depolarized cells. The importance of protein kinase C in regulating influx of Ca2+ was then evaluated. Addition of the phorbol ester 12-O-tetradecanoylphorbol 13-acetate prior to thapsigargin significantly decreased the influx of extracellular Ca2+. Studies with bisoxonol to measure membrane potential showed that TPA depolarized the plasma membrane in FRTL-5 cells. In cells where protein kinase C was downregulated or was inhibited by staurosporine, the thapsigargin-induced influx of Ca2+ was enhanced. The results indicate that emptying intracellular Ca2+ pools is sufficient to induce influx of Ca2+ in FRTL-5 cells, and that protein kinase C has a modulatory effect on this process.

Modulatory effect of protein kinase C on thapsigargin-induced calcium entry in thyroid FRTL-5 cells