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Intravenous prostaglandin E1 reduces monocyte chemoattractant protein-1 levels in peripheral arterial obstructive
Keiji Matsui1, Uichi Ikeda, Yoshiaki Murakami
1Division of Cardiovascular Medicine, Jichi Medical School, Tochigi, Japan.
Insights
Peripheral arterial obstructive disease (PAOD) patients have elevated monocyte chemoattractant protein-1 (MCP-1). Prostaglandin E1 (PGE1) treatment significantly reduced MCP-1 levels, suggesting a role in suppressing atherosclerotic lesion development.
Area of Science:
- Cardiovascular Science
- Immunology
- Pharmacology
Background:
- Monocytes are precursors to foam cells in atherosclerotic lesions.
- Monocyte chemoattractant protein-1 (MCP-1) is crucial for recruiting monocytes to vessel walls.
- Peripheral arterial obstructive disease (PAOD) involves monocyte activation.
Purpose of the Study:
- To measure serum MCP-1 levels in PAOD patients.
- To investigate the effect of intravenous prostaglandin E1 (PGE1) on MCP-1 levels in PAOD.
- To assess PGE1's potential to reduce atherosclerotic lesion development.
Main Methods:
- Eight PAOD patients (Fontaine stage II-IV) received daily intravenous PGE1 (10 microg) for 7 days.
- Serum samples were collected before and after PGE1 treatment.
- Assays included MCP-1, IL-6, hs-CRP, vWF, and ET-1.
Main Results:
- PAOD patients exhibited significantly higher serum MCP-1 levels compared to healthy controls (263.8 +/- 52.8 vs 136.5 +/- 15.0 pg/mL, P =.002).
- PGE1 treatment significantly decreased MCP-1 levels (from 263.8 +/- 52.8 to 196.1 +/- 25.5 pg/mL, P =.02).
- IL-6, hs-CRP, ET-1 levels, and vWF activity remained unaffected by PGE1 treatment.
Conclusions:
- Elevated serum MCP-1 in PAOD indicates monocyte activation in pathogenesis.
- Parenteral PGE1 administration reduced circulating MCP-1 levels.
- This reduction may suppress atherosclerotic lesion development in PAOD patients.
Objectives:
Blood monocytes are the precursors of the lipid-laden foam cells that are the hallmark of early atherosclerotic lesions, and monocyte chemoattractant protein-1 (MCP-1) plays important roles in their recruitment to the vessel wall. In this study, we measured serum levels of MCP-1 in patients with peripheral arterial obstructive disease (PAOD) and investigated whether intravenous prostaglandin E1 (PGE1) treatment, which produces clinical benefits in PAOD, might decrease such levels.
Methods:
Eight patients with PAOD at Fontaine stage II to IV were treated with a daily intravenous infusion of 10 microg of PGE1 for 7 consecutive days. Blood samples before and after 7-day PGE1 treatment were used for assays of MCP-1, interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), von Willebrand factor (vWF), and endothelin-1 (ET-1).
Results:
Serum MCP-1 levels in patients with PAOD were significantly higher than those in healthy control subjects (263.8 +/- 52.8 vs 136.5 +/- 15.0 pg/mL, P =.002). PGE1 administration for 7 days resulted in a significant decrease in the MCP-1 level, from 263.8 +/- 52.8 to 196.1 +/- 25.5 pg/mL (P =.02), whereas levels of IL-6, hs-CRP, and ET-1 and the activity of vWF were not affected.
Conclusions:
Serum MCP-1 levels were elevated in patients with PAOD, indicating the involvement of activation of monocytes in the pathogenesis of this disorder. Parenteral administration of PGE1 appeared to decrease circulating MCP-1 levels, which might lead to the suppression of the development of atherosclerotic lesions in patients with PAOD.