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J Biol Chem, Vol. 273, Issue 49, 32627-32635, December 4, 1998

Fatty Acid-mediated Calcium Sequestration within Intracellular Calcium Pools

From the Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland 21201

Intracellular Ca²⁺ pools play an essential role in generating Ca²⁺ signals. The heterogeneity of intracellular Ca²⁺ pools reflects the complex and dynamic character of the endoplasmic reticulum within which they reside. Translocation of Ca²⁺ between distinct subcompartments of the endoplasmic reticulum is mediated by a sensitive and specific GTP-activated process involving formation of reversible communicating junctions (Rys-Sikora, K. E., Ghosh, T. K., and Gill, D. L. (1994) J. Biol. Chem. 269, 31607-31613). In the presence of palmitate at 10 µM or above, this GTP-activated mechanism mediates substantial Ca²⁺ accumulation within a specific Ca²⁺-pumping pool. The fatty acid- and GTP-dependent accumulation of Ca²⁺ was highly chain length-specific; pentadecanoate (C₁₅) and palmitate (C₁₆) were equally effective, whereas fatty acids of shorter or longer chain length were either marginally effective or devoid of effect. Fatty acids with one or more unsaturated carbons were without effect, regardless of chain length. Palmitate-induced Ca²⁺ accumulation was immediately terminated with 2 µM palmitoyl-CoA, a blocker of the GTP-activated Ca²⁺-translocating mechanism. The anion transport inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid completely prevented both palmitate- and oxalate-mediated GTP-dependent Ca²⁺ accumulation, with EC₅₀ ~ 30 µM. Ca²⁺ sequestered in the presence of palmitate and GTP could be immediately and completely released by A23187, whereas the sequestered Ca²⁺ was remarkably resistant to release induced by inositol 1,4,5-trisphosphate (InsP₃). In contrast, oxalate-sequestered Ca²⁺ within the same pool could be effectively released by either ionophore or InsP₃. The results indicate that fatty acids are specifically transported into the lumen of a subset of Ca²⁺ pools, wherein they mediate substantial sequestration of Ca²⁺ in a distinct membrane-associated substate that is not readily releasable by opened InsP₃-sensitive Ca²⁺ channels.

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