Endothelial Activation

While endothelial disruption is a terminal event, endothelial activation is an adaptive response that is potentially reversible. Endothelial activation occurs in response to many immunologic and nonimmunologic stimuli. Many of the changes associated with endothelial activation are thought to be dependent on NFkB. Endothelial changes associated with activation include: (i) upregulation of surface expression of E-selectin, VCAM, class I and II MHC antigens; (ii) loss of surface proteins that are central in inhibiting coagulation such as thrombomodulin (TM, and heparan sulfate (HS); and (iii) release of cytokines and factors which are proinflammatory such as IL-, IL-1a and IL-8; release of factors which are procoagulant such as tissue factor (TF), plasminogen activator inhibitor type 1 (PAI-1), platelet activating factor (PAF); and (iii) and induction of enzymes such as inducible nitrous oxide synthetase (iNOS), or release of factors such as and Endothelin-1 which influence vasoactivity.

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