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  • Title: Lysophosphatidylcholine posttranscriptionally inhibits interferon-gamma-induced IP-10, Mig and I-Tac expression in endothelial cells.
    Author: Sheikh AM, Ochi H, Manabe A, Masuda J.
    Journal: Cardiovasc Res; 2005 Jan 01; 65(1):263-71. PubMed ID: 15621055.
    Abstract:
    OBJECTIVE: Lysophosphatidylcholine (lysoPC) is abundant in atherosclerotic lesions and has potential immunomodulatory activities. This study is aimed to investigate effects of lysoPC on the interferon (IFN)-gamma-induced gene expression, focusing on T cell-directed CXC chemokines relevant to atherosclerosis. METHODS AND RESULTS: Effects of lysoPC on the IFN gamma-induced gene expression of IFN-inducible protein of 10 kDa (IP-10), IFN-inducible T cell alpha chemoattractant (I-Tac), and monokine induced by IFN gamma (Mig) were evaluated in cultured endothelial cells. Northern blotting showed that lysoPC transiently and dose-dependently inhibited the IFN gamma-induced accumulation of IP-10, Mig and I-Tac but not p48, interferon regulatory factor-1 and guanidine binding protein-1. Nuclear run-off assays showed that lysoPC did not inhibit IP-10, Mig and I-Tac gene transcription. An analysis of the degradation of IP-10, Mig and I-Tac mRNA revealed it to be enhanced by lysoPC. CONCLUSION: LysoPC selectively inhibits IFN gamma-induced IP-10, I-Tac and Mig expression in endothelial cells, at least in part, by reducing mRNA stability. Thus, lysoPC might regulate T cell-mediated immunity by affecting IFN gamma-mediated activation of endothelial cells in atherosclerotic lesions.
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