Abstract
It is now accepted that lysophospholipids (LysoGPs) have a wide variety of functions as lipid mediators that are exerted through G protein-coupled receptors (GPCRs) specific to each lysophospholipid. While the roles of some LysoGPs, such as lysophosphatidic acid and sphingosine 1-phosphate, have been thoroughly examined, little is known about the roles of several other LysoGPs, such as lysophosphatidylserine (LysoPS), lysophosphatidylthreonine, lysophosphatidylethanolamine, lysophosphatidylinositol (LPI), and lysophosphatidylglycerol. Recently, a GPCR was found for LPI (GPR55) and three GPCRs (GPR34/LPS1, P2Y10/LPS2, and GPR174/LPS3) were found for LysoPS. In this review, we focus on these newly identified GPCRs and summarize the actions of LysoPS and LPI as lipid mediators.
Highlights
It is accepted that lysophospholipids (LysoGPs) have a wide variety of functions as lipid mediators that are exerted through G protein-coupled receptors (GPCRs) specific to each lysophospholipid
In the host-parasite interaction of schistosomes, LysoPS was identified as a Toll-like receptor 2 (TLR2)-activating molecule that prolonged the survival of the parasite and limited its pathology to the host [29]
Given that G␣13 signaling is induced by the three LysoPS receptors (P2Y10, A630033H20, and GPR174) which show similar expression patterns, it is likely that these three LysoPS receptors share redundant functions in activating the G␣13 pathway
Summary
LysoPS is known to induce several cellular responses both in vitro and in vivo (Fig. 2). LysoPS enhances histamine release from peritoneal rodent mast cells triggered by the cross-linking of high-affinity IgE receptors (FcRI). It induces rapid degranulation of mast cells and consequent anaphylactic shock and hypothermia when administered intravenously in rodents [21, 22]. The mast cell degranulation-stimulating activity is not induced by other LysoGPs including LPA, LPC, LPE, LPG, and LPI, and strictly requires the serine residue of LysoPS. It strictly requires the overall structure of the serine residue of LysoPS, because modification of the serine residue completely abolishes the mast cell degranulation-stimulating activity. In the host-parasite interaction of schistosomes, LysoPS was identified as a Toll-like receptor 2 (TLR2)-activating molecule that prolonged the survival of the parasite and limited its pathology to the host [29]
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