Pressure-Induced Vascular Activation of Nuclear Factor-κB

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Abstract
The effects of mechanical factors on nuclear factor (NF)-κB activation and its potential functional roles have been very little explored in the intact vessel. Thus, we chose to study the regulation of NF-κB by intraluminal pressure using an organ culture model of mouse carotid arteries maintained at 80 or 150 mm Hg during 24 hours. Gel shift analysis revealed an increase in the DNA-binding capacity of NF-κB in vessels at high pressure compared with vessels at normal pressure (304±49%; PPPP<0.001). These results were corroborated by immunohistochemical analysis showing positive staining for cleaved caspase 3 in vessels at 80 mm Hg treated with the NF-κB inhibitor peptide, which was additionally enhanced in treated vessels at 150 mm Hg. Our findings demonstrate that high intraluminal pressure activates NF-κB in arteries. Moreover, the activation of NF-κB seems to play a key role in preventing apoptosis in vascular cells, especially when vessels are exposed to high intraluminal pressure.