lysophosphatidylserine and Leukemia

In this study, we observed that lysophosphatidylserine (LPS) stimulated intracellular calcium ([Ca(2+)](i)) increase in leukemic cells but not in normal human peripheral blood mononuclear cells. LPS also stimulated [Ca(2+)](i) increase in human leukemic THP-1 cells. LPS-stimulated [Ca(2+)](i) increase was inhibited by U-73122 but not by U-73343. LPS also stimulated inositol phosphates formation in THP-1 cells, suggesting that LPS stimulates calcium signaling via phospholipase C activation. Moreover, pertussis toxin (PTX) completely inhibited [Ca(2+)](i) increase by LPS, indicating the activation of PTX-sensitive G-proteins. We also found that LPS-induced [Ca(2+)](i) increase was completely inhibited by suramin, suggesting G-protein coupled receptor activation. Since LPS specifically stimulates PTX-sensitive G-proteins, phospholipase C-dependent [Ca(2+)](i) increase in leukemic cells but not normal peripheral blood leukocytes, LPS receptor may be associated with leukemia.

Topics: Calcium; Cell Line, Tumor; Cells, Cultured; Dose-Response Relationship, Drug; GTP-Binding Proteins; Humans; Leukemia; Leukocytes, Mononuclear; Lysophospholipids; Pertussis Toxin; Receptors, Cell Surface; Receptors, G-Protein-Coupled; Receptors, Lysophosphatidic Acid