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Nitric oxide regulates monocyte chemotactic protein-1
1Division of Cardiovascular Medicine, Stanford University School of Medicine, Calif 94305-5246, USA.
Circulation
|August 5, 1997
Summary
Nitric oxide (NO) inhibits monocyte chemotactic protein-1 (MCP-1) expression, a key factor in atherosclerosis. This finding suggests NO
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Immunology
Background:
- Monocyte chemotactic protein-1 (MCP-1) is a critical chemokine for monocyte recruitment.
- Nitric oxide (NO) is known to inhibit monocyte-endothelial cell interactions and atherogenesis.
Purpose of the Study:
- To investigate the hypothesis that the antiatherogenic effect of NO is partly mediated by its inhibition of MCP-1 expression.
Main Methods:
- Studied MCP-1 expression and activity in smooth muscle cells (SMCs) exposed to LPS or oxidized LDL.
- Utilized NO donors and inhibitors in vitro and in vivo models (rabbits) to assess NO's regulatory role.
- Employed promoter activity assays and Northern analysis to confirm transcriptional regulation by NO.
Main Results:
- Oxidized LDL and LPS induced MCP-1 expression and NF-kappaB activation in SMCs.
- NO donors reduced MCP-1 induction and NF-kappaB activation.
- In vivo, NO inhibition increased MCP-1 expression, while NO supplementation decreased it in atherosclerotic rabbit aortas.
Conclusions:
- NO inhibits MCP-1 expression at the transcriptional level.
- NO's antiatherogenic effects may be partly attributed to its suppression of MCP-1.