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
- Authors
- Park B.[Park B.]; Yim J.-H.[Yim J.-H.]; Lee H.-K.[Lee H.-K.]; Kim B.-O.[Kim B.-O.]; Pyo S.[Pyo S.]
- Issue Date
- 2015
- Citation
- Bioscience, Biotechnology and Biochemistry, v.79, no.4, pp.539 - 542
- Journal Title
- Bioscience, Biotechnology and Biochemistry
- Volume
- 79
- Number
- 4
- Start Page
- 539
- End Page
- 542
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/47924
- DOI
- 10.1080/09168451.2014.991681
- 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 small interfering 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.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - Pharmacy > Department of Pharmacy > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.