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Inhibition of TNF‐α‐induced Adhesion Molecule Expression by Polar Lichen Extracts in mouse Vascular Smooth Muscle Cells via Downregulation of the JNK/p38 and NF‐κB Signaling Pathway
Author(s) -
Byeon Hyeeun,
Yim JoungHan,
Lee HongKum,
Pyo Suhkneung
Publication year - 2010
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.24.1_supplement.lb503
Subject(s) - p38 mitogen activated protein kinases , cell adhesion molecule , adhesion , downregulation and upregulation , cell adhesion , chemistry , vascular smooth muscle , microbiology and biotechnology , tumor necrosis factor alpha , nf κb , signal transduction , soluble cell adhesion molecules , cancer research , biology , immunology , smooth muscle , mapk/erk pathway , biochemistry , endocrinology , organic chemistry , gene
Adhesion of circulating leucocytes to the endothelial cell and their migration into arterial intima contribute to the inflammatory reaction as well as the formation of atherosclerotic lesions. Cellular adhesion molecules, which are rapidly induced by pro‐ atherosclerotic conditions, are responsible in such processes. Lichen‐derived compounds have been known to have a variety of biological activities, but the effect of polar lichen extracts (PLEs) on adhesion molecule expression is not known yet. In the present study, we examined whether PLEs are able to inhibit the expression of adhesion molecules induced by TNF‐α in mouse vascular smooth muscle cells (VSMCs). ELISA and immunoblotting analysis showed that PLE 1 suppressed the expression of VCAM‐1 and ICAM‐1 in surface and total cellular protein levels, while PLE 2 only attenuated VCAM‐1 expression. PLEs also abrogated NF‐κB activation and phosphorlyation of JNK and p38 induced by TNF‐α. Adhesion assay demonstrated that adhesion of monocytes to VSMCs was decreased by PLEs. Overall, these results suggest that PLEs downregulates TNF‐α‐induced adhesion molecule expression through the inhibition of JNK/p38 and NF‐κB signaling pathway and may be considered as a therapeutic strategy to reduce the risk of atherosclerosis.