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KMID : 0928520010110040453
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Korean Journal of Lipidology
2001 Volume.11 No. 4 p.453 ~ p.459
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Peroxisome Proliferator-Activated Receptor Gamma Mediated Inhibition of Plasminogen Activator Inhibitor Type 1 Expression of Human Umbilical Vein Endothelial Cells
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Hong Hye-Kyung
Cho Young-Min
Kim Min-Seon
Park Kyong-Soo
Lee Hong-Kyu
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Abstract
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Objective: Insulin resistance syndrome is a cluster of metabolic abnormalities including hyperglycemia, obesity, hypertension, dyslipidemia and hypercoagulability. The hypercoagulability is mainly caused by increased plasma level of plasminogen activator inhibitor type 1 (PAI-1) and is regarded as a risk factor of cardiovascular events. Peroxisome proliferator- activated receptor gamma (PPAR ) is a nuclear receptor, which regulates adipocyte differentiation and lipid metabolism. In human, PPAR agonist can decrease the plasma PAI-1 level, although this effect may be the indirect consequence of improved insulin sensitivity. However, the direct effect of PPAR on PAI-1 production in vascular endothelial cell is still unclear. In this study, we examined the role of PPAR on cultured human umbilical vein endothelial cell (HUVEC) focusing on PAI-1 production.
Methods: We examined the role of PPARγon PAI-1 expression in HUVEC with PPARγoverexpression and troglitazone (TRO) treatment. To determine the mRNA expression of PAI-1, we performed Northern hybridization. Also, we measured the effect of PPAR γon PAI-1 production during tumor necrosis factor (TNF ) treatment.
Results:TRO decreased PAI-1 production and its mRNA expression at the concentration of 5 g/mL. The inhibition of PAI-1 production by TRO was more pronounced in PPARγ-overexpressed HUVEC (p<0.05). TRO reduced the increase of PAI-1 production during TNF treatment and TRO showed a further reduction in PAI-1 production with PPARγoverexpression (p<0.05).
Conclusion: PPARγcan reduce the PAI-1 production in HUVEC and may prevent the increase of PAI-1 production during TNF treatment. These data suggest that PPARγplays a beneficial role in preventing cardiovascular events.
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KEYWORD
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Peroxisome proliferator-activated receptorγ, Endothelial cell, Plasminogen activator inhibitor type 1, Tumor necrosis factor α
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