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  • Title: Gene deletion of NF-kappaB p105 enhances neointima formation in a mouse model of carotid artery injury.
    Author: Ruusalepp A, Yan ZQ, Carlsen H, Czibik G, Hansson GK, Moskaug JØ, Blomhoff R, Valen G.
    Journal: Cardiovasc Drugs Ther; 2006 Apr; 20(2):103-11. PubMed ID: 16534546.
    Abstract:
    The role of nuclear factor kappa-B (NF-kappaB) p105 for vascular inflammatory gene expression and neointima formation after arterial injury was studied. Mice carotid arteries were injured by ligation. Vascular NF-kappaB activation was monitored using a NF-kappaB luciferase reporter mouse. Mice with gene deletion of the NF-kappaB p105 subunit (p50 precursor) and the corresponding wild types were assessed for vascular gene expression and neointimal hyperplasia. NF-kappaB was activated in the injured vessel wall in wild type mice, and this was accompanied by increased expression of the proinflammatory genes tumor necrosis factor alpha, interleukin 1 beta, and inducible nitric oxide synthase. In contrast, NF-kappaB p105 knockout mice had reduced expression of the inflammatory genes and enhanced neointima formation four weeks after ligation. Basic fibroblast growth factor (bFGF) gene expression increased after arterial ligation. A higher percentage of bFGF positive cells were found in lesions from NF-kappaB p105 knock out mice. These data indicate that the p105 subunit of NF-kappaB plays an essential role in vascular healing, and defects in NF-kappaB p105 promote neointima hyperplasia.
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