摘要
TNF-α is one of the most important proin-flammatory cytokines in mediating multiple physio-patho-logical functions during immunological responses. Vascular endothelial cells, when stimulated by TNF-α, can increase the expression of multiple cytokines and cellular adhesion molecules and, in turn, actively promote the inflammatory responses by recruiting and activating of leukocytes to the inflammatory site. In addition to endothelial death induced by TNF-α, we found for the first time that TNF-α can also induce the human endothelial cells senescence. The induced senescent endothelial cells will display SA-B-Gal staining and they were arrested in G0-G1 phase. We found that △(?)m would always be up-regulated in response to TNF-α stimula-tion at early time but when the cells become senescent, △(?)m shows a tendency to decrease. It may reflect the sthenic func-tion of mitochondria at early time in response to TNF-α stimulation and decay when the endothelial cells were in-duced senescent. ROS
TNF-α is one of the most important proin-flammatory cytokines in mediating multiple physio-patho-logical functions during immunological responses. Vascular endothelial cells, when stimulated by TNF-α, can increase the expression of multiple cytokines and cellular adhesion molecules and, in turn, actively promote the inflammatory responses by recruiting and activating of leukocytes to the inflammatory site. In addition to endothelial death induced by TNF-α, we found for the first time that TNF-α can also induce the human endothelial cells senescence. The induced senescent endothelial cells will display SA-B-Gal staining and they were arrested in G0-G1 phase. We found that △(?)m would always be up-regulated in response to TNF-α stimula-tion at early time but when the cells become senescent, △(?)m shows a tendency to decrease. It may reflect the sthenic func-tion of mitochondria at early time in response to TNF-α stimulation and decay when the endothelial cells were in-duced senescent. ROS fluctuates at early time and also de-creases when the endothelial cells become senescent. Our results show that the change of mitochondrial function may be related to the senescent process.
