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Figure 2. Non-mitochondrial, acidic compartment played a major role in the staurosporine-induced [Ca2+]c increase in rat submandibular acinar cells. Fura-2-loaded cells were stimulated with 10 µM carbachol, and perfusate Ca2+ was removed. Cells were then exposed to 100 nM ionomycin (n = 5; A) or 5 µM carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP; n = 4; B). Ionomycin and FCCP induced only small increases in [Ca2+]c, indicating that mitochondria did not contain sufficient Ca2+ to support staurosporine-induced [Ca2+]c increases. When cells were exposed to 10 µM monensin in the presence of 100 nM ionomycin, there was a large increase in [Ca2+]c (n = 9; C), suggesting that the acidic subcellular compartment contained a large amount of Ca2+. (D) Cells were stimulated with 10 µM carbachol, and perfusate Ca2+ was removed. Cells were then exposed to 200 nM staurosporine, causing the [Ca2+]c increase. When [Ca2+]c reached the maximum, 100 nM ionomycin was added, resulting in a decrease in [Ca2+]c to the basal level. Addition of 10 µM monensin in the presence of ionomycin did not induce an increase in [Ca2+]c, indicating that staurosproine released Ca2+ from the acidic compartment in rat submandibular acinar cells (n = 4).





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IADR Journals Advances in Dental Research ®
Journal of Dental Research ® Critical Reviews (1990-2004)