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

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...

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Veröffentlicht in:Journal of Pharmacological Sciences Jg. 100; H. 2; S. 162 - 166
Hauptverfasser: Shokawa, Tomoki, Yoshizumi, Masao, Yamamoto, Hideya, Omura, Shinji, Toyofuku, Mamoru, Shimizu, Yoshito, Imazu, Michinori, Kohno, Nobuoki
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Japan The Japanese Pharmacological Society 2006
Elsevier
Schlagworte:
Chemokine CCL2 - antagonists & inhibitors
Chemokine CCL2 - genetics
Dose-Response Relationship, Drug
Enzyme Induction
Gene Expression Regulation - drug effects
Heme Oxygenase-1 - biosynthesis
Heme Oxygenase-1 - genetics
Humans
Lysophosphatidylcholines - pharmacology
Monocytes - cytology
Monocytes - drug effects
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - metabolism
RNA, Ribosomal, 18S - metabolism
Time Factors
U937 Cells
ISSN:1347-8613
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Zusammenfassung: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.
Bibliographie:ObjectType-Article-2
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content type line 23
ISSN:1347-8613
DOI:10.1254/jphs.sc0040188