Chang Chi-Lun, Lin Mu-En, Hsu Hsien-Yeh, Yao Chao-Ling, Hwang Shiaw-Min, Pan Chien-Yuan, Hsu Chi-Yen, Lee Hsinyu
Institute of Zoology, National Taiwan University, Taipei, Taiwan.
J Biomed Sci. 2008 May;15(3):357-63. doi: 10.1007/s11373-007-9223-x. Epub 2007 Nov 25.
Lysophosphatidic acid (LPA), a low-molecular-weight lysophospholipid enriched in platelets and mildly oxidized low-density lipoproteins, is known to regulate inflammation and atherosclerosis by binding to its cognate receptors. In this study, we reported that LPA upregulated interleukin-1 beta (IL-1 beta) expression in mouse J774A.1 macrophages. By using pharmacological inhibitors, it was suggested that G(i)/Rho activation and subsequent reactive oxygen species (ROS) production were involved in IL-1 beta induction. In addition, IL-1 beta induction by LPA was also observed in human primary macrophages. In summary, LPA is involved in the processes of inflammation by affecting macrophage behavior.
溶血磷脂酸(LPA)是一种富含于血小板和轻度氧化的低密度脂蛋白中的低分子量溶血磷脂,已知其通过与其同源受体结合来调节炎症和动脉粥样硬化。在本研究中,我们报道LPA上调了小鼠J774A.1巨噬细胞中白细胞介素-1β(IL-1β)的表达。通过使用药理学抑制剂,提示G(i)/Rho激活以及随后的活性氧(ROS)产生参与了IL-1β的诱导。此外,在人原代巨噬细胞中也观察到LPA诱导IL-1β。总之,LPA通过影响巨噬细胞行为参与炎症过程。