Multiple actions of lysophosphatidylcholine in human Jurkat T cells

Aim:To obtain pathophysiological meanings of lysophosphatidylcholine(LPC)through the investigation of the effects of LPC in Jurkat T cells.Methods:Wemeasured ROS generation,[Ca2+]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 [Ca2+]iby Ca2+influx across the plasma membrane.However,LPC-inducedROS increase seemed to not be related with LPC-induced depolarization of MMPor [Ca2+]iincrease.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 [Ca2+]ithrough Ca2+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.