Cytokine-Induced Cell Surface Expression of Adhesion Molecules in Vascular Endothelial Cells In vitr

来源 :Journal of Tongji Medical University | 被引量 : 0次 | 上传用户:z3753091
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Regulation of the adhesion molecules expression by cytokine in vascular endothelial cells was investigated. Human umbilical vein endothelial cells (HUVEC) were stimulated with cytokines, TNF α (1-250 U/ml) or IL 1β (0.1-50 U/ml) for 24 h. HUVEC were also cultured with cytokines, TNF α (100 U/ml) or IL 1β (10 U/ml), for 4-72 h, cell surface expression of adhesion molecules (ICAM 1 and VCAM 1) were detected and quantitated by immunocytochemical methods and computerized imaging analysis technique. Adhesion molecules expression were up regulated by TNF α, IL 1β in a concentration and time dependent manner. Some significant differences were observed between the effects of cytokines on the ICAM 1 and on VCAM 1 expression. Cytokines might directly induce the expression of ICAM 1 and VCAM 1 in vascular endothelial cells. Our observations indicate differential functions of the two adhesion molecules during the evolution of inflammatory responses in stroke. Regulation of the adhesion molecule expression by cytokine in vascular endothelial cells was investigated. Human umbilical vein endothelial cells (HUVEC) were stimulated with cytokines, TNFα (1-250 U / ml) or IL 1β 24 h. HUVEC also also cultured with cytokines, TNFα (100 U / ml) or IL 1β (10 U / ml) for 4-72 h, cell surface expression of adhesion molecules (ICAM 1 and VCAM 1) were detected and Quantitated by immunocytochemical methods and computerized imaging analysis technique. Adhesion molecules expression were up regulated by TNFα, IL 1β in a concentration and time dependent manner. Some significant differences were observed between the effects of cytokines on the ICAM 1 and on VCAM 1 expression. Cytokines might directly induce the expression of ICAM 1 and VCAM 1 in vascular endothelial cells. Our profiles indicate the differential functions of the two adhesion molecules during the evolution of inflammatory responses in stroke.
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