Gene Deletion of NF-κB p105 Enhances Neointima Formation in a Mouse Model of Carotid Artery Injury

Author： Ruusalepp Arno Yan Zhong-Qun Carlsen Harald Czibik Gabor Hansson Göran Moskaug Jan-Øyvind Blomhoff Rune Valen Guro

Publisher： Springer Publishing Company

ISSN： 0920-3206

Source： Cardiovascular Drugs and Therapy, Vol.20, Iss.2, 2006-04, pp. : 103-111

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Abstract

The role of nuclear factor kappa-B (NF-κB) p105 for vascular inflammatory gene expression and neointima formation after arterial injury was studied. Mice carotid arteries were injured by ligation. Vascular NF-κB activation was monitored using a NF-κB luciferase reporter mouse. Mice with gene deletion of the NF-κB p105 subunit (p50 precursor) and the corresponding wild types were assessed for vascular gene expression and neointimal hyperplasia. NF-κB 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-κB 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-κB p105 knock out mice. These data indicate that the p105 subunit of NF-κB plays an essential role in vascular healing, and defects in NF-κB p105 promote neointima hyperplasia.