Modulation of vascular inflammation in vitro and in vivo by peroxisome proliferator-activated receptor-gamma activators
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Summary
This summary is machine-generated.Peroxisome proliferator-activated receptor-gamma (PPARgamma) activators reduce inflammatory markers like VCAM-1 and ICAM-1 in endothelial cells. These compounds also significantly decrease monocyte/macrophage accumulation in atherosclerotic plaques, suggesting therapeutic potential.
Area Of Science
- Cardiovascular Research
- Immunology
- Endocrinology
Background
- Peroxisome proliferator-activated receptor-gamma (PPARgamma) is present in atherosclerotic plaques and endothelial cells.
- The impact of PPARgamma activators on endothelial activation and plaque inflammation is not well understood.
Purpose Of The Study
- To investigate the effect of PPARgamma activators on vascular cell adhesion molecule (VCAM-1) and intercellular adhesion molecule (ICAM-1) expression in endothelial cells.
- To determine if PPARgamma activators reduce monocyte/macrophage homing to atherosclerotic plaques in vivo.
Main Methods
- Cultured endothelial cells were treated with PPARgamma agonists (troglitazone, 15d-PGJ2) and stimulated with tumor necrosis factor.
- VCAM-1 and ICAM-1 expression were quantified using flow cytometry.
- ApoE-deficient mice received troglitazone treatment to assess monocyte/macrophage homing to atherosclerotic plaques.
Main Results
- PPARgamma agonists significantly attenuated tumor necrosis factor-induced VCAM-1 and ICAM-1 expression in endothelial cells.
- Troglitazone treatment dose-dependently reduced monocyte/macrophage homing to atherosclerotic plaques in apoE-deficient mice.
- E-selectin and PECAM-1 expression remained unchanged.
Conclusions
- PPARgamma activators effectively inhibit VCAM-1 and ICAM-1 expression in activated endothelial cells.
- These findings indicate that PPARgamma activators can significantly reduce inflammatory cell recruitment in atherosclerosis.
- PPARgamma activators may offer therapeutic benefits for managing inflammatory responses in atherosclerosis.