M Okada1, T Matsuto, T Miida, K Inano. 1. Department of Laboratory Medicine, Niigata University School of Medicine, Japan.
Abstract
OBJECTIVES: Expressions of adhesion molecules on arterial endothelial cells are crucial events in initiation of atherosclerosis. Our recent study has shown that endothelial cells express endothelial leukocyte adhesion molecule-1 (ELAM-1) significantly due to stimulation with oxidized LDL, H2O2, or hypoxia. This current study is aimed at investigating temporal relations of the induction of ELAM-1, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in cultured endothelial cells of the human thoracic aorta. METHODS: The activators examined were interleukin 1 alpha (IL-1 alpha), tumor necrosis factor alpha (TNF alpha), and interferon gamma (IFN gamma). Cells were incubated with each of the cytokines at 10 ng/ml for 0.5-48 hours. The adhesion molecules were determined by enzyme immunoassay. RESULTS: ELAM-1 appeared after stimulations by IL-1 and TNF alpha; ELAM-1 was induced by IL-1 after one hour, while it rose sharply after a 30-min stimulation by TNF alpha. The ICAM-1 expression was observed even in non-stimulated cells and further increased in proportion to duration of stimulation. No significant difference occurred between the effects of IL-1 and TNF alpha on the ICAM-1 expression. Weak expression of VCAM-1 was observed only by TNF alpha after 4-through 24-h stimulation. IFN gamma did not cause any changes in the expression of ELAM-1, VCAM-1, and ICAM-1. CONCLUSIONS: The present data indicate a specific time course for each induction of ELAM-1 and VCAM-1, but not ICAM-1. Therefore, the combination of molecules may play a role for endothelial cells to discriminate monocytes from such other cells as neutrophils and lymphocytes.
OBJECTIVES: Expressions of adhesion molecules on arterial endothelial cells are crucial events in initiation of atherosclerosis. Our recent study has shown that endothelial cells express endothelial leukocyte adhesion molecule-1 (ELAM-1) significantly due to stimulation with oxidized LDL, H2O2, or hypoxia. This current study is aimed at investigating temporal relations of the induction of ELAM-1, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in cultured endothelial cells of the human thoracic aorta. METHODS: The activators examined were interleukin 1 alpha (IL-1 alpha), tumor necrosis factor alpha (TNF alpha), and interferon gamma (IFN gamma). Cells were incubated with each of the cytokines at 10 ng/ml for 0.5-48 hours. The adhesion molecules were determined by enzyme immunoassay. RESULTS:ELAM-1 appeared after stimulations by IL-1 and TNF alpha; ELAM-1 was induced by IL-1 after one hour, while it rose sharply after a 30-min stimulation by TNF alpha. The ICAM-1 expression was observed even in non-stimulated cells and further increased in proportion to duration of stimulation. No significant difference occurred between the effects of IL-1 and TNF alpha on the ICAM-1 expression. Weak expression of VCAM-1 was observed only by TNF alpha after 4-through 24-h stimulation. IFN gamma did not cause any changes in the expression of ELAM-1, VCAM-1, and ICAM-1. CONCLUSIONS: The present data indicate a specific time course for each induction of ELAM-1 and VCAM-1, but not ICAM-1. Therefore, the combination of molecules may play a role for endothelial cells to discriminate monocytes from such other cells as neutrophils and lymphocytes.
Authors: Ming Wai Hung; Hang Mee Yeung; Chi Fai Lau; Angela Ming See Poon; George L Tipoe; Man Lung Fung Journal: Int J Mol Sci Date: 2017-05-24 Impact factor: 5.923