title: Lysophosphatidylserine stimulates chemotactic migration in U87 human glioma cells.
abstract: Lysophosphatidylserine (LPS) was found to stimulate intracellular calcium increase in U87 human glioma cells. LPS also stimulated chemotactic migration of U87 human glioma cells, which was completely inhibited by pertussis toxin (PTX). Moreover, LPS was also found to stimulate ERK, p38 MAPK, JNK, and Akt activities in U87 cells. We observed that LPS-induced U87 chemotaxis was mediated by PI3K, p38 MAPK, and JNK. LPS-induced chemotactic migration in U87 cells was inhibited by Ki16425, an LPA(1/3) receptor-selective antagonist, which suggested that the Ki16425-sensitive G-protein coupled receptor (GPCR) played a role in this process. Moreover, U87 cells were found to uniquely express LPA(1) but not LPA(2-5). In addition, LPS failed to stimulate the NF-kappaB-driven luciferase activity in exogenously LPA(1)-transfected HepG2 cells. Taken together, we propose that LPS stimulates GPCR, which is in contrast to the well-known LPA receptors, thus resulting in the chemotactic migration in U87 human glioma cells.
authors.affiliation: Department of Biochemistry, College of Medicine, Dong-A University, 3-1 Dongdaesindong Seogu, Busan 602-714, Republic of Korea.
authors.forename: Sun Young
authors.initials: SY
authors.lastname: Lee
authors.forename: Ha-Young
authors.initials: HY
authors.lastname: Lee
authors.forename: Sang Doo
authors.initials: SD
authors.lastname: Kim
authors.forename: Seong Ho
authors.initials: SH
authors.lastname: Jo
authors.forename: Jae Woong
authors.initials: JW
authors.lastname: Shim
authors.forename: Hye-Jeong
authors.initials: HJ
authors.lastname: Lee
authors.forename: Jeanho
authors.initials: J
authors.lastname: Yun
authors.forename: Yoe-Sik
authors.initials: YS
authors.lastname: Bae
mesh_terms: D001932:Brain Neoplasms / Q000378:metabolism*; D045744:Cell Line, Tumor; D002633:Chemotaxis / Q000187:drug effects; D005910:Glioma / Q000378:metabolism*; D006801:Humans; D007555:Isoxazoles / Q000494:pharmacology; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008246:Lysophospholipids / Q000494:pharmacology / Q000502:physiology*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D011422:Propionates / Q000494:pharmacology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000819:agonists* / Q000037:antagonists & inhibitors / Q000378:metabolism; D049368:Receptors, Lysophosphatidic Acid / Q000235:genetics / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: C477898:3-(4-(4-((1-(2-chlorophenyl)ethoxy)carbonyl amino)-3-methyl-5-isoxazolyl) benzylsulfanyl) propanoic acid; D007555:Isoxazoles; D008246:Lysophospholipids; D011422:Propionates; D043562:Receptors, G-Protein-Coupled; D049368:Receptors, Lysophosphatidic Acid; C025059:lysophosphatidylserine; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases