Modulation of C-Reactive Protein–Mediated Monocyte Chemoattractant Protein-1 Induction in Human Endothelial Cells by Anti-Atherosclerosis Drugs
Key result
CRP induced a 7-fold increase in MCP-1 secretion in human endothelial cells, an effect that was significantly inhibited by simvastatin and fenofibrate but not by aspirin.
Why the study?
Do anti-atherosclerosis drugs modulate CRP-induced MCP-1 secretion in human endothelial cells?
Population
Cultured human umbilical vein endothelial cells
Comparison
Recombinant human CRP with or without… vs Control (no CRP) or CRP alone
Design
Preclinical
Authors
Discussion
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Implication
Supports pleiotropic anti-inflammatory effects of statins and fibrates in vitro; leaves open clinical translation in atherosclerosis.
Key Points
- This research aims to investigate the effects of C-reactive protein on chemokine production in endothelial cells and the modulation by anti-atherosclerosis medications.
- Cultured human umbilical vein endothelial cells were treated with varying concentrations of recombinant human CRP.
- Chemokine secretion was measured using ELISA to quantify MCP-1 and RANTES levels.
- The influence of anti-atherosclerosis drugs, including aspirin, simvastatin, fenofibrate, and ciglitazone, on MCP-1 induction was assessed.
- At 100 microgram/mL CRP, MCP-1 secretion increased 7-fold (baseline < 100 pg/mL), p<0.001.
- Simvastatin (5 micromol/L) significantly inhibited MCP-1 induction compared to control, p<0.005.
- Fenofibrate (100 micromol/L) almost completely abolished MCP-1 induction, while ciglitazone had a moderate effect.
Structured PICO
Do anti-atherosclerosis drugs modulate CRP-induced MCP-1 secretion in human endothelial cells?
P
Population
Cultured human umbilical vein endothelial cells
I
Intervention
Recombinant human CRP (5-100 microgram/mL) with or without anti-atherosclerosis drugs (aspirin, simvastatin, fenofibrate, Wy-14649, ciglitazone)
C
Comparator
Control (no CRP) or CRP alone
O
Outcome
Secretion of chemokines MCP-1 and RANTESsurrogate
Simvastatin and fenofibrate inhibit CRP-induced MCP-1 secretion in human endothelial cells, suggesting a novel anti-inflammatory mechanism for these drugs.
Cite This Study
Pasceri et al. (2001) studied Vascular inflammation. C-reactive protein and anti-atherosclerosis drugs was evaluated on Secretion of chemokines MCP-1 and RANTES. CRP induced a 7-fold increase in MCP-1 secretion in human endothelial cells, an effect that was significantly inhibited by simvastatin and fenofibrate but not by aspirin.