Expression of NF-kappa B and I kappa B-alpha by aortic endothelium in an arterial injury model.

摘要: Endothelial cells at sites of inflammatory responses express a variety genes that are under the control nuclear factor NF-kappa B, transcription with its inhibitors may be linked in an autoregulatory system can activated by multiple signals relevant to vascular pathophysiology. A model limited endothelial denudation aorta rats and mice was used study role B inhibitor I kappa B-alpha Using en face techniques for situ hybridization immunostaining, normal endothelium showed diffuse cytoplasmic immunoreactivity components p50 p65 as well Within 45 minutes after wounding, staining both noticeable wound edge, which followed dramatic induction VCAM-1 mRNA protein 3 hours later. Leading edge also responded up-regulated expression B-alpha. The increased p50, p65, VCAM-1, persisted replicating associated adhesion monocyte/macrophages these cells. Expression levels returned regeneration. Our data establish first time presence B/I vasculature demonstrate correlation between activation regulatory B-dependent molecule animal arterial injury. This important homeostatic mechanism vessel wall.