Role of Nuclear Factor-κB and Protein Kinase C Signaling in the Expression of the Kinin B1 Receptor in Human Vascular Smooth Muscle Cells

2006 ◽  
Vol 71 (3) ◽  
pp. 949-956 ◽  
Author(s):  
Marie Eve Moreau ◽  
Marie-Thérèse Bawolak ◽  
Guillaume Morissette ◽  
Albert Adam ◽  
François Marceau
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Vascular Smooth Muscle Cells ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
B1 Receptor ◽  
Kinase C ◽  
Kinin B1 Receptor

scholarly journals Homocysteine stimulates nuclear factor κB activity and monocyte chemoattractant protein-1 expression in vascular smooth-muscle cells: a possible role for protein kinase C

2000 ◽  
Vol 352 (3) ◽  
pp. 817-826 ◽  
Author(s):  
Guoping WANG ◽  
Yaw L. SIOW ◽  
Karmin O
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Vascular Smooth Muscle Cells ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Kinase C

Monocyte chemoattractant protein-1 (MCP-1) is a potent chemokine that stimulates the migration of monocytes into the intima of arterial walls. Although many factors that induce MCP-1 expression have been identified, the effect of homocysteine on the expression of MCP-1 in atherogenesis and the underlying mechanisms are not entirely clear. The objective of the present study was to investigate the role of homocysteine in MCP-1 expression in human aorta vascular smooth-muscle cells (VSMCs). After VSMCs were incubated with homocysteine for various time periods, a nuclease protection assay and ELISA were performed. Homocysteine (0.05Ő0.2mM) significantly increased the expression of MCP-1 mRNA (up to 2.7-fold) and protein (up to 3.3-fold) in these cells. The increase in MCP-1 expression was associated with the activation of protein kinase C (PKC) as well as nuclear factor κB (NF-κB). Further investigation demonstrated that the activation of NF-κB was the result of a PKC-mediated reduction in the expression of inhibitory protein (IκBα) mRNA and protein in homocysteine-treated cells. Oxidative stress might also be involved in the activation of NF-κB by homocysteine in VSMCs. In conclusion, the present study has clearly demonstrated that the activation of PKC as well as superoxide production followed by activation of NF-κB is responsible for homocysteine-induced MCP-1 expression in VSMCs. These results suggest that homocysteine-stimulated MCP-1 expression via NF-κB activation may play an important role in atherogenesis.

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