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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Ichiki, Tomoko Takenoshita, Yoko Jougasaki, Michihisa Setoguchi, Manabu |
| Description | Author Affiliation: Jougasaki M ( Institute for Clinical Research, National Hospital Organization Kagoshima Medical Center, Kagoshima, Japan. michi@qjun.hosp.go.jp) |
| Abstract | BACKGROUND AND PURPOSE: The mechanisms of anti-inflammatory actions of statins, 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase inhibitors, remain unclear. We investigated the effects of statins on interleukin (IL)-6-induced monocyte chemo-attractant protein (MCP)-1 expression and monocyte chemotaxis. EXPERIMENTAL APPROACH: Cultures of human aortic endothelial cells (HAECs) were stimulated with IL-6 in the absence and presence of statins. Gene expression and protein secretion of MCP-1, phosphorylation of Janus kinase (JAK) and the signal transducers and activators of transcription (STAT) pathway, and human monocyte migration were examined. KEY RESULTS: IL-6 plus its soluble receptor sIL-6R (IL-6/sIL-6R) promoted THP-1 monocyte migration, and increased gene expression and protein secretion of MCP-1, more than IL-6 alone or sIL-6R alone. Various statins inhibited IL-6/sIL-6R-promoted monocyte migration and MCP-1 expression in HAECs. Co-incubation of mevalonate and geranylgeranyl pyrophosphate, but not farnesyl pyrophosphate, reversed the inhibitory effects of statins on MCP-1 expression. Geranylgeranyl transferase inhibitor, but not farnesyl transferase inhibitor, suppressed IL-6/sIL-6R-stimulated MCP-1 expression. IL-6/sIL-6R rapidly phosphorylated JAK1, JAK2, TYK2, STAT1 and STAT3, which were inhibited by statins. Transfection of STAT3 small interfering RNA (siRNA), but not STAT1 siRNA, attenuated the ability of IL-6/sIL-6R to enhance THP-1 monocyte migration. In addition, statins blocked IL-6/sIL-6R-induced translocation of STAT3 to the nucleus. CONCLUSIONS AND IMPLICATIONS: Statins suppressed IL-6/sIL-6R-induced monocyte chemotaxis and MCP-1 expression in HAECs by inhibiting JAK/STAT signalling cascades, explaining why statins have anti-inflammatory properties beyond cholesterol reduction. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 6 |
| Volume Number | 159 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 2010-03-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Chemokine CCL2 Biosynthesis Endothelial Cells Drug Effects Endothelium, Vascular Hydroxymethylglutaryl-CoA Reductase Inhibitors Pharmacology Interleukin-6 Janus Kinases Antagonists & Inhibitors Transcriptional Activation Aorta Cytology Enzymology Immunology Metabolism Cells, Cultured Genetics Chemotaxis, Leukocyte Enzyme Inhibitors Immunohistochemistry Phosphorylation Signal Transduction Research Support, Non-U.S. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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