Induction of Heme Oxygenase-1 Inhibits Monocyte Chemoattractant Protein-1 mRNA Expression in U937 Cells

DOI Web Site 被引用文献3件 参考文献19件
  • Shokawa Tomoki
    Department of Molecular and Internal Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Japan
  • Yoshizumi Masao
    Department of Cardiovascular Physiology and Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Japan
  • Yamamoto Hideya
    Department of Molecular and Internal Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Japan
  • Omura Shinji
    Department of Biomedical Chemistry, Graduate School of Biomedical Sciences, Hiroshima University, Japan
  • Toyofuku Mamoru
    Department of Molecular and Internal Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Japan
  • Shimizu Yoshito
    Department of Molecular and Internal Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Japan
  • Imazu Michinori
    Department of Molecular and Internal Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Japan
  • Kohno Nobuoki
    Department of Molecular and Internal Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Japan

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抄録

Heme oxygenase-1 (HO-1) is a stress-inducible isoform of HO with potential cytoprotective effects. Monocyte activation/migration mediated by monocyte chemoattractant protein-1 (MCP-1) is one of the earliest and important events in the pathogenesis of atherosclerosis. We examined the effect of HO-1 on the production of lysophosphatidylcholine (Lyso-PC)-induced MCP-1 in the human promonocytic cell line U937. Increased HO-1 induction by hemin resulted in a significant decrease in the Lyso-PC-mediated induction of MCP-1 mRNA expression. SnPP (IX), the specific inhibitor of HO-1 enzymatic activity, prevented the hemin-mediated attenuation of MCP-1 mRNA expression. These results suggest that HO-1 may work as an anti-atherogenic agent through the attenuation of MCP-1 production.<br>

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