Literature DB >> 20014193

Overexpression of activated nuclear factor-kappa B in aorta of patients with coronary atherosclerosis.

Wei Zhang1, Shan Shan Xing, Xue Lin Sun, Qi Chong Xing.   

Abstract

BACKGROUND: Inflammation is an established risk factor for atherosclerosis. In an inflammatory state, nuclear factor-kappa B (NF-kappaB) is frequently activated as a key transcription activator for the downstream responses. HYPOTHESIS: The aim of this study was to investigate the changes of NF-kappaB in the aorta of patients with coronary atherosclerosis and its association with atherosclerotic risk factors.
METHODS: From 2004 to 2005, we collected a small piece of ascending aorta in the bypass procedure from patients (n = 31) undergoing coronary artery bypass graft (CABG) surgery. The expression of NF-kappaB was determined by immunohistochemistry, and its transcriptional activity was evaluated by electrophoretic mobility shift assay. Celiac aortic tissues from 4 subjects without known atherosclerosis through the kidney donation program were taken as control.
RESULTS: NF-kappaB was detectable in aortas from CABG patients with the transcriptional activities significantly increased. The relative level of aortic NF-kappaB expression was elevated in patients who were smokers or with hypertension. Spearman correlation revealed that aortic NF-kappaB expression had significant correlation with coronary severity scores (Gensini score, r = 0.608, P < .05). The NF-kappaB expression was positively correlated with the levels of blood glucose, low-density lipoprotein cholesterol, lipoprotein(a), total cholesterol, and non-high-density lipoprotein cholesterol (P < .05); but negatively correlated with high-density lipoprotein cholesterol (P < .05).
CONCLUSIONS: Our study demonstrates a highly activated NF-kappaB in aortas from patients with coronary atherosclerosis, which may reflect overall arterial overinflammatory status. The findings of hyperactive NF-kappaB in aortas may provide a diagnostic parameter for the inflammation that is associated with and may cause atherosclerosis. Copyright 2009 Wiley Periodicals, Inc.

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Year:  2009        PMID: 20014193      PMCID: PMC6652953          DOI: 10.1002/clc.20482

Source DB:  PubMed          Journal:  Clin Cardiol        ISSN: 0160-9289            Impact factor:   2.882


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