**7. Other relevant biological actions of C1P**

In a previous report, Hinkovska-Galcheva et al (Hinkovska-Galcheva et al., 1998) showed that endogenous C1P can be generated during the phagocytosis of antibody-coated erythrocytes in human neutrophils that were primed with formylmethionylleucylphenylalanine. More recently, the same group demonstrated that C1P is a key mediator of neuthophil phagocytosis (Hinkovska-Galcheva et al., 2005). In addition, it was reported that C1P can be formed in neutrophils upon incubation with cell-permeable [3H]*N*-hexanoylsphingosine (C6-ceramide) (Rile et al., 2003), and Riboni and co-workers (Riboni et al., 2002) found that C1P can be generated in cerebellar granule cells both from SM-derived ceramide and through the recycling of sphingosine produced by ganglioside catabolism. C1P can be also generated by the action of interleukin 1-betta on A549 lung adenocarcinoma cells (Pettus et al., 2003b), or by stimulation of bone marrow-derived macrophages with macrophage-colony stimulating factor (M-CSF) (Gangoiti et al., 2008b). We found that C1P is present in normal bone marrow-derived macrophages isolated from healthy mice (Gomez-Munoz et al., 2004), and that C1P levels are substantially decreased in apoptotic macrophages. These observations are consistent with recent findings showing that CerK plays a key role in the stimulation of cell proliferation in A549 human lung adenocarcinoma cells (Mitra et al., 2007), and the induction of neointimal formation via cell proliferation and cell cycle progression in vascular smooth muscle cells by C1P (Kim et al., 2011).
