Lysophosphatidylcholine-induced taurine release in HeLa cells involves protein kinase activity.
It has recently been demonstrated that exogenous addition of low concentrations (< 15 microM) of lysophosphatidyl choline ( LPC, palmitic acid in the sn-1 position) induces a transient increase in taurine efflux from HeLa cells in a process that seems to involve generation of reactive oxygen species (ROS) and tyrosine phosphorylation (J. Membrane Biol. 176 (2000) 175-185). We now demonstrate that LPC also induces release of taurine under isotonic conditions in mouse fibroblast (NIH/3T3) and Ehrlich ascites tumor cells. Furthermore, we show that in the case of HeLa cells addition of the calmodulin antagonist W-7 (50 microM) or the calmodulin-dependent kinase II (CaMKII) inhibitor KN-62 (10 microM) reduces the LPC-induced taurine release under isotonic conditions. Conversely, addition of a standard protein kinase C (PKC) inhibitor chelerythrine (10 microM) leads to a potentiation of the LPC-induced taurine efflux, whereas direct activation of PKC by the phorbol ester PMA has no effect. It is suggested that the putative generation of ROS following addition of LPC is modulated by calmodulin/CaMKII, and that the effect of chelerythrine is more likely related to the ROS production than to PKC inhibition.[1]References
- Lysophosphatidylcholine-induced taurine release in HeLa cells involves protein kinase activity. Lambert, I.H., Falktoft, B. Comp. Biochem. Physiol., Part A Mol. Integr. Physiol. (2001) [Pubmed]
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