Lee Sun Young, Lee Ha-Young, Kim Sang Doo, Jo Seong Ho, Shim Jae Woong, Lee Hye-Jeong, Yun Jeanho, Bae Yoe-Sik
Department of Biochemistry, College of Medicine, Dong-A University, 3-1 Dongdaesindong Seogu, Busan 602-714, Republic of Korea.
Biochem Biophys Res Commun. 2008 Sep 12;374(1):147-51. doi: 10.1016/j.bbrc.2008.06.117. Epub 2008 Jul 9.
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.
溶血磷脂酰丝氨酸（LPS）被发现可刺激U87人胶质瘤细胞内钙离子增加。LPS还可刺激U87人胶质瘤细胞的趋化性迁移，而百日咳毒素（PTX）可完全抑制这种迁移。此外，还发现LPS可刺激U87细胞中的ERK、p38丝裂原活化蛋白激酶（MAPK）、JNK和Akt活性。我们观察到LPS诱导的U87趋化性是由磷脂酰肌醇-3激酶（PI3K）、p38 MAPK和JNK介导的。LPA(1/3)受体选择性拮抗剂Ki16425可抑制LPS诱导的U87细胞趋化性迁移，这表明对Ki16425敏感的G蛋白偶联受体（GPCR）在此过程中发挥了作用。此外，发现U87细胞独特地表达LPA(1)，而不表达LPA(2 - 5)。此外，LPS未能刺激外源性转染LPA(1)的HepG2细胞中NF-κB驱动的荧光素酶活性。综上所述，我们提出LPS刺激GPCR，这与众所周知的溶血磷脂酸（LPA）受体不同，从而导致U87人胶质瘤细胞的趋化性迁移。
