TNF-related activation-induced cytokine enhances leukocyte adhesiveness: Induction of ICAM-1 and VCAM-1 via TNF receptor-associated factor and protein kinase c-dependent NF-kappa B activation in endot
SCIE
SCOPUS
- Title
- TNF-related activation-induced cytokine enhances leukocyte adhesiveness: Induction of ICAM-1 and VCAM-1 via TNF receptor-associated factor and protein kinase c-dependent NF-kappa B activation in endot
- Authors
- Min, JK; Kim, YM; Kim, SW; Kwon, MC; Kong, YY; Hwang, IK; Won, MH; Rho, J; Kwon, YG
- Date Issued
- 2005-07-01
- Publisher
- AMER ASSOC IMMUNOLOGISTS
- Abstract
- Inflammation is a basic pathological mechanism leading to a variety of vascular diseases. The inflammatory reaction involves complex interactions between both circulating and resident leukocytes and the vascular endothelium. In this study, we report evidence for a novel action of TNF-related activation-induced cytokine (TRANCE) as an inflammatory mediator and its underlying signaling mechanism in the vascular wall. TRANCE significantly increased endothelial-leukocyte cell interactions, and this effect was associated with increased expression of the cell adhesion molecules, ICAM-1 and VCAM-1, on the endothelial cells. RT-PCR analysis and promoter assays revealed that expression of these cell adhesion molecules was transcriptionally regulated mainly by activation of the inflammatory transcription factor, NF-kappa B. TRANCE induced I kappa B-alpha phosphorylation and NF-kappa B activation via a cascade of reactions involving the TNFR-associated factors, phospholipase C, PI3K, and protein kinase C (PKC-alpha and PKC-zeta). It also led to the production of reactive oxygen species via PKC- and PI3K-dependent activation of NADPH oxidase in the endothelial cells, and antioxidants suppressed the responses to TRANCE. These results demonstrate that TRANCE has an inflammatory action and may play a role in the pathogenesis of inflammation-related diseases.
- Keywords
- INTERCELLULAR-ADHESION MOLECULE-1; OSTEOCLAST DIFFERENTIATION FACTOR; NECROSIS-FACTOR-ALPHA; FIBROBLAST-GROWTH-FACTOR; OSTEOPROTEGERIN LIGAND; GENE-EXPRESSION; VASCULAR CALCIFICATION; TERMINAL KINASE; DENDRITIC-CELL; FAMILY-MEMBER
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/24525
- DOI
- 10.4049/jimmunol.175.1.531
- ISSN
- 0022-1767
- Article Type
- Article
- Citation
- JOURNAL OF IMMUNOLOGY, vol. 175, no. 1, page. 531 - 540, 2005-07-01
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