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A novel cyclin-dependent kinase inhibitor down-regulates tumor necrosis factor-α (TNF-α)-induced expression of cell adhesion molecules by inhibition of NF-κB activation in human pulmonary epithelial cells

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Author(s)
Jung Hwa OhEun Jung ParkJong-Wook ParkJinho LeeSang Han LeeTaeg Kyu Kwon
Keimyung Author(s)
Park, Jong WookKwon, Taeg Kyu
Department
Dept. of Immunology (면역학)
Journal Title
International Immunopharmacology
Issued Date
2010
Volume
10
Issue
5
Abstract
BAI (a novel cyclin-dependent kinase (CDK) inhibitor, 2-[1,1′-biphenyl]-4-yl-N-[5-(1,1-dioxo-1λ6-isothiazolidin-
2-yl)-1H-indazol-3-yl] acetamide) is known to have anti-proliferative activity, but the mechanismresponsible for
it remains unclear. We here investigated the functional effect of BAI on airway inflammation and its action
mechanism. BAI down-regulated the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell
adhesion molecule-1 (VCAM-1) in human lung epithelial A549 cells stimulated with tumor necrosis factor-α:
(TNF-α), resulting in the suppression of leukocyte adhesion to lung epithelial A549 cells. In addition, BAI inhibited
TNF-α-induced expression of adhesion molecules (ICAM-1 and VCAM-1) protein andmRNA in a dose-dependent
manner. BAI inhibited nuclear factor-κB (NF-κB) activity and nuclear translocation of NF-κB. Furthermore, BAI
potently inhibits the TNF-α-induced increase in ROS generation in A549 cells, suggesting that inhibition of ROS
generation is maybe involved in the BAI-mediated inhibition of TNF-α-induced ICAM-1 down-regulation to A549
cells. Taken together, these results suggest that BAI inhibits cell adhesion through inhibition of ICAM-1 and VCAM-
1 expressions, at least in part, by inhibition of ROS generation and down-regulation of NF-κB activity.
© 2010 Elsevier B.V. All rights reserved.
Keimyung Author(s)(Kor)
박종욱
권택규
Publisher
School of Medicine
Citation
Jung Hwa Oh et al. (2010). A novel cyclin-dependent kinase inhibitor down-regulates tumor necrosis factor-α
(TNF-α)-induced expression of cell adhesion molecules by inhibition of NF-κB
activation in human pulmonary epithelial cells. International Immunopharmacology, 10(5), 572–579. doi: 10.1016/j.intimp.2010.02.004
Type
Article
ISSN
1567-5769
Source
https://www.sciencedirect.com/science/article/pii/S1567576910000639?via%3Dihub
DOI
10.1016/j.intimp.2010.02.004
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/35957
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
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