Acta Pharmacologica Sinica 2006 June; 27 (6): 700-707; doi: 10.1111/j.1745-7254.2006.00339.x

Aim: To obtain pathophysiological meanings of lysophosphatidylcholine (LPC)through the investigation of the effects of LPC in Jurkat T cells .

Methods: We measured ROS generation, [Ca²⁺]_i, and mitochondrial membrane potential (MMP)by fluorescent spectrometry in Jurkat T cells.

Results: We observed that LPC significantly increased the reactive oxygen species (ROS) level in human Jurkat T cells. Among structurally-related lysolipids and eleven synthetic LPCs with different acyl chain lengths, palmitoyl LPC increased ROS to the highest level. a-Tocopherol, an antioxidant, and rottlerin PKCd inhibitor were inhibitory effects on LPC-induced ROS generation. LPC rapidly depolarized MMP and markedly elevated [Ca²⁺]_i by Ca²⁺ influx across the plasma membrane. However, LPC-induced ROS increase seemed to not be related with LPC-induced depolarization of MMP or [Ca²⁺]_i increase. G2A family G protein-coupled receptors (GPCR) for lysolipids were expressed in Jurkat T cells, however, evidence indicated that GPCR was not involved in LPC actions.

Conclusion: LPC induced several cellular changes in Jurkat T cells, including an increase of ROS generation in a PKCd-dependent and GPCR-independent manner, increase of [Ca²⁺]_i through Ca²⁺ 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 intracellular signaling molecules.

Keywords: lysophosphatidylcholine; reactive oxygen species; calcium; protein kinase C; mito-chondrial membrane potential