https://scholars.lib.ntu.edu.tw/handle/123456789/468559
標題: | Superoxide dismutase inhibits the expression of vascular cell adhesion molecule-1 and intracellular cell adhesion molecule-1 induced by tumor necrosis factor-α in human endothelial cells through the JNK/p38 pathways | 作者: | Lin S.-J. Shyue S.-K. Hung Y.-Y. Chen Y.-H. Ku H.-H. Chen J.-W. Tam K.-B. YUH-LIEN CHEN |
公開日期: | 2005 | 卷: | 25 | 期: | 2 | 起(迄)頁: | 334-340 | 來源出版物: | Arteriosclerosis, Thrombosis, and Vascular Biology | 摘要: | Objective - Expression of adhesion molecules on endothelial cells and subsequent leukocyte recruitment are critical early events in the development of atherosclerosis. We tried to study possible effects of Cu/Zn superoxide dismutase (SOD) on adhesion molecule expression and its underlying mechanism in the prevention and treatment of cardiovascular disorders. Methods and Results - Human aortic endothelial cells (HAECs) were transfected with adenovirus carrying the human SOD gene (AdSOD) to investigate whether SOD expression in HAECs attenuated tumor necrosis factor (TNF)-α-induced reactive oxygen species production and adhesion molecule expression and to define the mechanisms involved. SOD expression significantly suppressed TNF-α-induced expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 and reduced the binding of the human neutrophils to TNF-α-stimulated HAECs. SOD expression suppressed c-JUN N-terminal kinase and p38 phosphorylation. It also attenuated intracellular superoxide anion production and NADPH oxidase activity in TNF-α-treated HAECs. Conclusions - These results provide evidence that SOD expression in endothelial cells attenuates TNF-α-induced superoxide anion production and adhesion molecule expression, and that this protective effect is mediated by decreased JNK and p38 phosphorylation and activator protein-1 and nuclear factor κB inactivation. These results suggest that SOD has antiinflammatory properties and may play important roles in the prevention of atherosclerosis and inflammatory response. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-13244270147&doi=10.1161%2f01.ATV.0000152114.00114.d8&partnerID=40&md5=57d0eea5f861135a0a1861bd9c08f404 https://scholars.lib.ntu.edu.tw/handle/123456789/468559 |
ISSN: | 1079-5642 | DOI: | 10.1161/01.ATV.0000152114.00114.d8 | SDG/關鍵字: | adenovirus vector; copper zinc superoxide dismutase; immunoglobulin enhancer binding protein; intercellular adhesion molecule 1; mitogen activated protein kinase p38; reactive oxygen metabolite; reduced nicotinamide adenine dinucleotide phosphate oxidase; stress activated protein kinase; superoxide; transcription factor AP 1; tumor necrosis factor alpha; vascular cell adhesion molecule 1; antiinflammatory activity; aorta; article; atherosclerosis; cardiovascular disease; cell adhesion; endothelium cell; enzyme phosphorylation; gene expression; genetic transfection; human; human cell; leukocyte; neutrophil; priority journal; protein expression; viral gene therapy; Anthracenes; Aorta; Arteriosclerosis; Cell Adhesion; Depression, Chemical; Endothelial Cells; Endothelium, Vascular; Flavonoids; Gene Expression Regulation; Humans; Imidazoles; Inflammation; Intercellular Adhesion Molecule-1; JNK Mitogen-Activated Protein Kinases; MAP Kinase Signaling System; NADPH Oxidase; Neutrophils; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Protein Processing, Post-Translational; Pyridines; Recombinant Fusion Proteins; Superoxide Dismutase; Superoxides; Transcription Factor AP-1; Transcription, Genetic; Transduction, Genetic; Tumor Necrosis Factor-alpha; Vascular Cell Adhesion Molecule-1 |
顯示於: | 解剖學暨細胞生物學科所 |
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