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Aim:To obtain pathophysiological meanings of lysophosphatidylcholine(LPC)through the investigation of the effects of LPC in Jurkat T cells.Methods:Wemeasured ROS generation,[Ca~(2+)]_i,and mitochondrial membrane potential(MMP)by fluorescent spectrometry in Jurkat,T cells.Results:We observed that LPCsignificantly increased the reactive oxygen species(ROS)level in human Jurkat Tcells.Among structurally-related lysolipids and eleven synthetic LPCs with dif-ferent acyl chain lengths,palmitoyl LPC increased ROS to the highest level,α-Tocopherol,an antioxidant,and rottlerin PKCδ inhibitor were inhibitory effects onLPC-induced ROS generation.LPC rapidly depolarized MMP and markedly el-evated [Ca~(2+)]_i by Ca~(2+)influx across the plasma membrane.However,LPC-inducedROS increase seemed to not be related with LPC-induced depolarization of MMPor [Ca~(2+)]_i increase.G2A family G protein-coupled receptors(GPCR)for lysolipidswere expressed in Jurkat T cells,however,evidence indicated that GPCR was notinvolved in LPC actions.Conclusion:LPC induced several cellular changes inJurkat T cells,including an increase of ROS generation in a PKCδ-dependent andGPCR-independent manner,increase of [Ca~(2+)]_i through Ca~(2+)influx,and decreaseof MMP.LPC-induced actions in Jurkat T cells represent novel action modes ofLPC that do not involve GPCR and multiple independent changes of intracellularsignaling molecules.
Aim: To obtain pathophysiological meanings of lysophosphatidylcholine (LPC) through the investigation of the effects of LPC in Jurkat T cells. Methods: Wemeasured ROS generation, [Ca ~ (2 +)] _i, and mitochondrial membrane potential (MMP) by fluorescent spectrometry in Jurkat, T cells. Results: We observed that LPCs slightly increased the reactive oxygen species (ROS) level in human Jurkat T cells. Am structural structurally-related lysolipids and eleven synthetic LPCs with dif-ferent acyl chain lengths, palmitoyl LPC increased ROS to the highest level, α-Tocopherol, an antioxidant, and rottlerin PKCδ inhibitor were inhibitory effects on LPC-induced ROS generation.LPC rapidly depolarized MMP and markedly el-evated [Ca ~ (2 +)] i by Ca 2+ influx across the Plasma membrane. However, LPC-inducedROS increase seemed to not be related to LPC-induced depolarization of MMPor [Ca2 +] _i increase. G2A family G protein-coupled receptors (GPCRs) for lysolipidswere expressed in Jurkat T cells, however, evidence indicates that GPCR w as notinvolved in LPC actions.Conclusion: LPC induced several cellular changes in Jurkat T cells, including an increase of ROS generation in a PKCδ-dependent and GPCR-independent manner, increase of [Ca ~ (2 +)] _i through Ca ~ (2+ ) influx, and decrease of MMP. LPC-induced actions in Jurkat T cells represent novel action modes of LPC that do not involve GPCR and multiple independent changes of intracellularsignaling molecules.