title: Lysophosphatidylcholine upregulates LOX-1, chemokine receptors, and activation-related transcription factors in human T-cell line Jurkat.
abstract: In arteriosclerosis, activated T cells infiltrating the atherosclerotic lesions are directly involved in the pathogenesis of these vascular disorders. Infiltration and accumulation of T cells into the vascular wall occur at the earliest stage of atherosclerosis. The atherosclerotic lesion also sees the accumulation of modified lipids such as lysophosphatidylcholine (lysoPC), the main phospholipid component of oxidized low-density lipoprotein. However, it remains less clear how lysoPC affects CD4 T cells. Therefore, we assessed the effect of lysoPC on various mRNA expressions in human T cells using real-time quantitative Reverse Transcription-PCR. Exposure of Jurkat cells (a human CD4 T-cell line) to lysoPC resulted in upregulation of CXCR4 and CCR5 chemokine receptors, receptor for oxidized low-density lipoprotein (LOX-1), the transcription factors, nuclear factor-kappa beta (NF-kB) and Yin Yang 1, and target molecules of NF-kB, A1/Bfl1/BCL2A1 and c-IAP1/BIRC2, in a dose-dependent manner. These data indicate that lysoPC is a positive regulator of the inflammatory response in human CD4 T cells. Further, it suggested that lysoPC and CD4 T cells accumulating in atherosclerotic lesions contribute to the development of arteriosclerosis.
authors.affiliation: Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
authors.forename: Yuko
authors.initials: Y
authors.lastname: Hara
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Kusumi
authors.forename: Masako
authors.initials: M
authors.lastname: Mitsumata
authors.forename: Xiao-Kang
authors.initials: XK
authors.lastname: Li
authors.forename: Masayuki
authors.initials: M
authors.lastname: Fujino
mesh_terms: D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism; D049109:Cell Proliferation; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins / Q000378:metabolism; D019169:Jurkat Cells; D008244:Lysophosphatidylcholines / Q000378:metabolism*; D015778:Minor Histocompatibility Antigens; D016328:NF-kappa B / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D019713:Receptors, CCR5 / Q000378:metabolism; D019718:Receptors, CXCR4 / Q000378:metabolism; D019707:Receptors, Chemokine / Q000235:genetics / Q000378:metabolism*; D051127:Scavenger Receptors, Class E / Q000235:genetics / Q000378:metabolism*; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*; D015533:Transcriptional Activation; D015854:Up-Regulation; D050986:YY1 Transcription Factor / Q000378:metabolism
chemical_list: C096816:BCL2-related protein A1; C527276:CXCR4 protein, human; D051034:Inhibitor of Apoptosis Proteins; D008244:Lysophosphatidylcholines; D015778:Minor Histocompatibility Antigens; D016328:NF-kappa B; C495137:OLR1 protein, human; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D019713:Receptors, CCR5; D019718:Receptors, CXCR4; D019707:Receptors, Chemokine; D051127:Scavenger Receptors, Class E; D014157:Transcription Factors; D050986:YY1 Transcription Factor; C494698:YY1 protein, human