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Activated platelets induce secretion of interleukin-1beta, monocyte chemotactic protein-1, and macrophage inflammatory protein-1alpha and surface expression of intercellular adhesion molecule-1 on cultured endothelial cells
Journal of Korean Medical Science ; : 273-278, 2000.
Artículo en Inglés | WPRIM | ID: wpr-132629
ABSTRACT
Atherosclerosis is an inflammatory disease. Platelet-endothelium interaction plays an important role in the pathophysiology of atherogenesis. We investigated the role of activated platelets for secretion of interleukin (IL)-1beta, monocyte chemotactic protein (MCP)-1 and macrophage inflammatory protein (MIP)-1alpha and expression of intercellular adhesion molecule (ICAM)-1 on endothelial cells. Human umbilical vein endothelial cells (HUVEC) were incubated with non-stimulated or ADP-activated platelets for 6 hr. Secretion of interleukin (IL)-1beta, MCP-1 and MIP-1alpha and surface expression of ICAM-1 were measured by ELISA and flow cytometry. In the presence of activated platelets, the secretion of IL-1beta, MCP-1, and MIP-1alpha and surface expression of ICAM-1 were significantly increased compared with non-activated platelets. The present study shows that activated platelets may contribute to expression of various inflammatory mediators on endothelial cells.
Asunto(s)

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Plaquetas / Endotelio Vascular / Activación Plaquetaria / Células Cultivadas / Interleucina-1 / Molécula 1 de Adhesión Intercelular / Quimiocina CCL2 / Proteínas Inflamatorias de Macrófagos Límite: Humanos Idioma: Inglés Revista: Journal of Korean Medical Science Año: 2000 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Plaquetas / Endotelio Vascular / Activación Plaquetaria / Células Cultivadas / Interleucina-1 / Molécula 1 de Adhesión Intercelular / Quimiocina CCL2 / Proteínas Inflamatorias de Macrófagos Límite: Humanos Idioma: Inglés Revista: Journal of Korean Medical Science Año: 2000 Tipo del documento: Artículo