Norepinephrine mediates differential activation of NF-κB and subsequent proatherogenic gene expression

Abstract

Background: Diabetes mellitus places considerable psychologic stress on the affected individuals. Psychosocial factors are associated with the development and progress of cardiovascular disease, but the pathological mechanisms are yet not clear. In previous work, we have identified norepinephrine (NE)- mediated activation of the proinflammatory transcription factor NF-κB in mononuclear cells as a pathway that converts psychosocial stress into cellular activation. Since this action requires a cooperated action of both α and β adrenergic receptors, we hypothesized that a differential activation of NFκB subunits might underlie the catecholamine-dependent expression of different proatherogenic genes.