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Multiple actions of lysophosphatidylcholine in human Jurkat T cells

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Abstract:

Abstract

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. α-Tocopherol, an antioxidant, and rottlerin PKC 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 PKC-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: calcium; lysophosphatidylcholine; mitochondrial membrane potential; protein kinase C; reactive oxygen species

Document Type: Research Article

DOI: https://doi.org/10.1111/j.1745-7254.2006.00339.x

Affiliations: 1: Laboratories of Pharmacology, College of Pharmacy and Research Institute for Drug Development, Pusan National University, Busan 609-735, Korea 2: Aging Biochemistry, College of Pharmacy and Research Institute for Drug Development, Pusan National University, Busan 609-735, Korea

Publication date: 2006-06-01

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