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Park, B./ J.-H. Yim/ H.-K. Lee/ B.-O. Kim/ S. Pyo 2015: Ramalin inhibits VCAM-1 expression and adhesion of monocyte to vascular smooth muscle cells through MAPK and PADI4-dependent NF-κB and AP-1 pathways. - Bioscience, Biotechnology and Biochemistry 79(4): 539-542. [RLL List # 239 / Rec.# 36215]
Keywords: Inflammation/ PADI4/ Ramalin/ Transcription factor/ Biomolecules/ Cell adhesion/ Cell culture/ Cytology/ Diseases/ Molecules/ Transcription factors/ Adhesion molecules/ Inflammation/ Monocytic leukemia cells/ PADI4/ Ramalin/ Reactive oxygen species/ Vascular cell adhesion molecule-1/ Vascular Smooth Muscle Cells/ Cells/ Ramalina
Abstract: Cell adhesion molecules play a critical role in inflammatory processes and atherosclerosis. In this study, we investigated the effect of ramalin, a chemical compound from the Antarctic lichen Ramalina terebrata, on vascular cell adhesion molecule-1 (VCAM-1) expression induced by TNF- α in vascular smooth muscular cells (VSMCs). Pretreatment of VSMCs with ramalin (0.1-10 μg/mL) concentrationdependently inhibited TNF- α-induced VCAM-1 expression. Additionally, ramalin inhibited THP-1 (human acute monocytic leukemia cell line) cell adhesion to TNF- α-stimulated VSMCs. Ramalin suppressed TNF-α-induced production of reactive oxygen species (ROS), PADI4 expression, and phosphorylation of p38, ERK, and JNK. Moreover, ramalin inhibited TNF-α -induced translocation of NF-κB and AP-1. Inhibition of PADI4 expression by smallinterfering RNA or the PADI4-specific inhibitor markedly attenuated TNF-α-induced activation of NF-κB and AP-1 and VCAM-1 expression in VSMCs. Our study provides insight into the mechanisms underlying ramalin activity and suggests that ramalin may be a potential therapeutic agent to modulate infl ammation within atherosclerosis. © 2014 Japan Society for Bioscience, Biotechnology, and Agrochemistry.KW
URL: http://dx.doi.org/10.1080/09168451.2014.991681
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