{'fraction_non_alphanumeric': 0.022519352568613652, 'fraction_numerical': 0.00211118930330753, 'mean_word_length': 6.004926108374384, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
IKKβ‐dependent NF‐κB pathway controls vascular inflammation and intimal hyperplasia

Nuclear factor‐κB (NF‐κB)‐mediated vascular inflammation is a prominent characteristic of atherogenesis and restenosis. We noted that angioplastic injury to carotid artery elicited two phases of NF‐κB activation characterized by an early activation in the arterial media and a late activation coupled with high levels of inhibitor of IκB kinase (IKK) activity in intima. These findings prompted us to elucidate the role for the different phases of NF‐κB activation and IKK in the progress of vascular repair. Our results show that blockade of the early NF‐κB activation by perivascular administration of pyrrolidine dithiocarbamate transiently attenuates the expression of proinflammatory genes in the injured vessels but does not affect intimal formation. Interruption of IKKβ by overexpressing a dominant‐negative IKKβ in the injured artery effectively inhibited the late phase of NF‐κB activation, resulting in down‐regulation of inducible nitric oxide synthase, tumor necrosis factor α, and monocyte chemoattractant protein‐1 expression in conjunction with a 36% reduction in intima size, albeit with a lack of inhibitory effect on the early NF‐κB activation. Collectively, these findings show that the IKKβ‐mediated late‐phase NF‐κB activation contributes to intimal hyperplasia and the accompanied vascular inflammatory responses.