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Department of Biomedical Sciences and Italian Research Council (CNR) Center for the Study of Biomembranes, University of
Padova, 35121 Padova, Italy
The functional characteristics of a nonacidic,
inositol 1,4,5-trisphosphate- and thapsigargin-insensitive Ca2+ pool have been characterized in mammalian
cells derived from the rat pituitary gland (GH3, GC,
and GH3B6), the adrenal tissue (PC12), and mast cells
(RBL-1). This Ca2+ pool is released into the cytoplasm
by the Ca2+ ionophores ionomycin or A23187 after the
discharge of the inositol 1,4,5-trisphosphate-sensitive
store with an agonist coupled to phospholipase C activation and/or thapsigargin. The amount of Ca2+
trapped within this pool increased significantly after a
prolonged elevation of intracellular Ca2+ concentration
elicited by activation of Ca2+ influx. This pool was affected neither by caffeine-ryanodine nor by mitochondrial uncouplers. Probing mitochondrial Ca2+ with recombinant aequorin confirmed that this pool did not
coincide with mitochondria, whereas its homogeneous
distribution across the cytosol, as revealed by confocal
microscopy, and its insensitivity to brefeldin A make localization within the Golgi complex unlikely. A proton
gradient as the driving mechanism for Ca2+ uptake was
excluded since ionomycin is inefficient in releasing Ca2+ from acidic pools and Ca2+ accumulation/release
in/from this store was unaffected by monensin or
NH4Cl, drugs known to collapse organelle acidic pH
gradients. Ca2+ sequestration inside this pool, thus, may
occur through a low-affinity, high-capacity Ca2+-ATPase
system, which is, however, distinct from classical endosarcoplasmic reticulum Ca2+-ATPases. The cytological
nature and functional role of this Ca2+ storage compartment are discussed.
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