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In Jurkat T cells, the anti-CD3 antibody OKT3 and thapsigargin (TG) elevated the cytoplasmic free Ca2+ concentration ([Ca2+]i), after which it decreased to a sustained, elevated level. In contrast, lysophosphatidic acid (LPA) increased [Ca2+]i only briefly and transiently, after which it declined to the resting level of [Ca2+]i even in the presence of extracellular Ca2+. OKT3 increased Ins(1,4,5)P3 formation but neither LPA nor TG did. In the absence of extracellular Ca2+, the addition of OKT3 did not affect an elevation of [Ca2+]i induced by the subsequent addition of LPA and vice versa. In permeabilized Jurkat cells, the addition of Ins(1,4,5)P3 released Ca2+; this was inhibited by heparin, whereas LPA released Ca2+ even in the presence of heparin. cADP-ribose released Ca2+; this was additive with LPA-induced Ca2+ release and vice versa in permeabilized Jurkat cells. LPA did not stimulate Ca2+ entry and 45Ca2+ uptake but OKT3 and TG did. LPA, OKT3 and TG did not affect the sustained elevation of [Ca2+]i induced by ionomycin. The present results suggest that at least three kinds of intracellular Ca2+ stores, which are Ins(1,4,5)P3,-cADP-ribose- and LPA-sensitive, exist in Jurkat T cells, and that the LPA-sensitive intracellular Ca2+ store does not regulate Ca2+ entry at the plasma membrane.

Lysophosphatidic acid-sensitive intracellular Ca2+ store does not regulate Ca2+ entry at plasma membrane in Jurkat human T-cells