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D-myo-inositol 1,3,4,5-tetrakisphosphate releases Ca2+ from crude microsomes and enriched vesicular plasma membranes, but not from intracellular stores of permeabilized T-lymphocytes and monocytes.

ABSTRACT: In the human T-lymphocyte cell lines Jurkat and HPB.ALL and the human monocytoid cell line U937, Ins(1,3,4,5)P4 triggers a dose-dependent release of Ca2+ from crude microsomal preparations, with a half-maximal effective concentration (EC50) of 1.2-2.3 microM. Similar results were obtained with enriched vesicular plasma membranes from U937 cells. However, in permeabilized preparations of the same cell types only Ins(1,4,5)P3 was able to release Ca2+ from intracellular stores, with EC50 values in the range 0.11-0.84 microM. In crude microsomes the effects of Ins(1,3,4,5)P4 and Ins(2,4,5)P3, a non-metabolizable InsP3 isomer, occurred independently of each other, indicating subpopulations of Ins(1,3,4,5)P4- and Ins(1,4,5)P3-sensitive vesicles. The Ins(1,3,4,5)P4 preparation used for the Ca(2+)-release experiments contains neither Ca2+ nor contaminating Ins(1,4,5)P3 and was not metabolized to Ins(1,4,5)P3 during the Ca(2+)-release experiments. We conclude that Ins(1,3,4,5)P4 independently of Ins(1,4,5)P3 induces a Ca2+ flux via a membrane compartment, most likely the plasma membrane, that is functionally destroyed during the permeabilization of the cells.

SUBMITTER: Guse AH

PROVIDER: S-EPMC1132037 | biostudies-other | 1992 Dec

REPOSITORIES: biostudies-other

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Project description:L1210 lymphoma cells were permeabilized with digitonin, and the ability of Ins(2,4,5)P3 and Ins(1,3,4,5)P4 to mobilize intracellular Ca2+ was studied. At high doses of Ins(2,4,5)P3 Ca2+ was rapidly released from intracellular stores, and prior or subsequent addition of Ins(1,3,4,5)P4 had no discernible effect. However, the Ca2(+)-mobilizing action of low (threshold or just above) concentrations of Ins(2,4,5)P3 was markedly enhanced by Ins(1,3,4,5)P4, which alone caused no mobilization of Ca2+; this phenomenon was shown not to be due to protection of Ins(2,4,5)P3 by the Ins(1,3,4,5)P4 against hydrolysis. The ability of the pre-addition of Ins(1,3,4,5)P4 to enhance subsequent Ins(2,4,5)P3-induced Ca2+ mobilization was always seen whether or not the free Ca2+ concentration was low (pCa = 7) or high (pCa = 6). However, at low Ca2+, Ins(1,3,4,5)P4 could cause a further mobilization if added after the Ins(2,4,5)P3, whereas at higher Ca2+ values Ins(1,3,4,5)P4 was only able to affect Ca2+ if added before Ins(2,4,5)P3. These effects of Ins(1,3,4,5)P4 were not, at the same concentration, mimicked by a random mixture of InsP4 isomers obtained by partial acid hydrolysis of phytic acid, by Ins(1,3,4)P3 or by Ins(1,3,4,5,6)P5, and they were shown not to be due to enzymic generation of Ins(1,4,5)P3 from Ins(1,3,4,5)P4 by (a) the absence of any detectable production of Ins(1,4,5)P3 if radiolabelled Ins(1,3,4,5)P4 was used, or (b) the observation that Ins(1,3,4,5,6)P5 could mimic Ins(1,3,4,5)P4 provided that higher doses were used; this inositol phosphate, when added radiolabelled, yielded only trace quantities of D/L-Ins(1,4,5,6)P4, which itself does not mobilize Ca2+. We interpret these results overall to mean that in these cells there is a small proportion of the Ins(2,4,5)P3-mobilizable Ca2+ pools which can only be mobilized in the presence of Ins(1,3,4,5)P4 [or at the least, Ins(1,3,4,5)P4 can help Ins(2,4,5)P3 to gain access to them]. The significance of this conclusion is discussed in the light of current concepts of the second messenger function of Ins(1,3,4,5)P4.

Dataset Information

D-myo-inositol 1,3,4,5-tetrakisphosphate releases Ca2+ from crude microsomes and enriched vesicular plasma membranes, but not from intracellular stores of permeabilized T-lymphocytes and monocytes.

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