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Journal of atherosclerosis and thrombosis

The atherogenic effects of serum amyloid A are potentially mediated via inflammation and apoptosis.


PMID 24785395

Abstract

The mechanism through which SAA contributes to the pathogenesis of atherosclerosis remains unclear. The objective of this study was therefore to determine whether SAA plays a role in the onset of atherosclerosis via inflammatory and apoptotic pathways. An array of experiments, including cell cultures, MTT assays, quantitative real-time PCR and Western blotting, were carried out in order to assess the effects of human recombinant SAA on NF-κB activation and the role of NF-κB in the onset of SAA-induced inflammation and apoptosis. We found that SAA (80μg/mL) induced 3.5- to 37.8-fold increases in the expression of targets known to play important roles in the initiation and progression of atherosclerosis (i.e., ICAM-1, MCP-1, MMP-9 and TF) via NF-κB regulation within one hour after exposure. RAW264.7 cells treated with increasing doses of SAA showed regulation of apoptotic targets and a dose-dependent reduction in cell viability, with 69% cell viability observed following exposure to 80μg/mL of SAA for 24 hours. Our results suggest that SAA contributes to the pathogenesis of atherosclerosis via both inflammatory and apoptotic mechanisms.