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IL‐4 induces interleukin‐6 (IL‐6) expression in human aortic endothelial cells
Author(s) -
Lee Yong Woo,
Lee Won Hee
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.964.3
Subject(s) - pyrrolidine dithiocarbamate , inflammation , endothelium , interleukin , cytokine , immunology , biology , medicine , chemistry , nf κb
Previous studies have demonstrated that the pro‐oxidative and pro‐inflammatory pathways within vascular endothelium play an important role in the initiation and progression of atherosclerosis. The present study was designed to examine the hypothesis that interleukin‐4 (IL‐4) may up‐regulate expression of pro‐inflammatory cytokine IL‐6 in human aortic endothelial cells (HAEC). Quantitative real‐time RT‐PCR and enzyme‐linked immunosorbent assay (ELISA) showed that exposure of HAEC to IL‐4 significantly up‐regulated the mRNA and protein expression of IL‐6. Overexpression of IL‐6 was further confirmed in aorta and serum isolated from IL‐4‐injected mice. In addition, pretreatment with antioxidants, such as pyrrolidine dithiocarbamate (PDTC) and epigallocatechin gallate (EGCG), significantly and dose‐dependently inhibited IL‐4‐induced IL‐6 expression in HAEC. These results suggest that IL‐4 can induce IL‐6 expression through antioxidant‐sensitive mechanisms in human aortic endothelial cells. These data may contribute to understanding the cellular and molecular mechanisms involved in IL‐4‐mediated progression of atherosclerosis and development of therapeutic strategies for the prevention of atherosclerotic lesion development specifically targeted against inflammatory pathways. (This work was supported by Grant Number R15HL085229 from the National Heart, Lung, and Blood Institute)