A mechanism converting psychosocial stress into mononuclear cell activation

• Verfasst von: Bierhaus, Angelika [VerfasserIn]
• Verfasst von: Wolf, Jutta [VerfasserIn]
• Verfasst von: Andrassy, Martin [VerfasserIn]
• Verfasst von: Rohleder, Nicolas [VerfasserIn]
• Verfasst von: Humpert, Per Magnus [VerfasserIn]
• Verfasst von: Petrov, Dimitri [VerfasserIn]
• Verfasst von: Ferstl, Roman [VerfasserIn]
• Verfasst von: Eynatten, Maximilian von [VerfasserIn]
• Verfasst von: Wendt, Thoralf Manfred [VerfasserIn]
• Verfasst von: Rudofsky, Gottfried [VerfasserIn]
• Verfasst von: Joswig, Martina [VerfasserIn]
• Verfasst von: Morcos, Michael [VerfasserIn]
• Verfasst von: Schwaninger, Markus [VerfasserIn]
• Verfasst von: McEwen, Bruce [VerfasserIn]
• Verfasst von: Kirschbaum, Clemens [VerfasserIn]
• Verfasst von: Nawroth, Peter Paul [VerfasserIn]
• Titel: A mechanism converting psychosocial stress into mononuclear cell activation
• Verf.angabe: Angelika Bierhaus, Jutta Wolf, Martin Andrassy, Nicolas Rohleder, Per M. Humpert, Dimitri Petrov, Roman Ferstl, Maximilian von Eynatten, Thoralf Wendt, Gottfried Rudofsky, Martina Joswig, Michael Morcos, Markus Schwaninger, Bruce McEwen, Clemens Kirschbaum, and Peter P. Nawroth
• E-Jahr: 2003
• Jahr: February 10, 2003
• Umfang: 6 S.
• Teil: volume:100
• Teil: year:2003
• Teil: number:4
• Teil: pages:1920-1925
• Teil: extent:6
• Fussnoten: Gesehen am 29.03.2021
• Titel Quelle: Enthalten in: National Academy of Sciences (Washington, DC)Proceedings of the National Academy of Sciences of the United States of America
• Ort Quelle: Washington, DC : National Acad. of Sciences, 1915
• Jahr Quelle: 2003
• Band/Heft Quelle: 100(2003), 4, Seite 1920-1925
• ISSN Quelle: 1091-6490
• DOI: doi:10.1073/pnas.0438019100
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1752660935

Abstract

Little is known about the mechanisms converting psychosocial stress into cellular dysfunction. Various genes, up-regulated in atherosclerosis but also by psychosocial stress, are controlled by the transcription factor nuclear factor κB (NF-κB). Therefore, NF-κB is a good candidate to convert psychosocial stress into cellular activation. Volunteers were subjected to a brief laboratory stress test and NF-κB activity was determined in peripheral blood mononuclear cells (PBMC), as a window into the body and because PBMC play a role in diseases such as atherosclerosis. In 17 of 19 volunteers, NF-κB was rapidly induced during stress exposure, in parallel with elevated levels of catecholamines and cortisol, and returned to basal levels within 60 min. To model this response, mice transgenic for a strictly NF-κB-controlled β-globin transgene were stressed by immobilization. Immobilization resulted in increased β-globin expression, which could be reduced in the presence of the α1-adrenergic inhibitor prazosin. To define the role of adrenergic stimulation in the up-regulation of NF-κB, THP-1 cells were induced with physiological amounts of catecholamines for 10 min. Only noradrenaline resulted in a dose- and time-dependent induction of NF-κB and NF-κB-dependent gene expression, which depended on pertussis-toxin-sensitive G protein-mediated phosphophatidylinositol 3-kinase, Ras/Raf, and mitogen-activated protein kinase activation. Induction was reduced by α1- and β-adrenergic inhibitors. Thus, noradrenaline-dependent adrenergic stimulation results in activation of NF-κB in vitro and in vivo. Activation of NF-κB represents a downstream effector for the neuroendocrine response to stressful psychosocial events and links changes in the activity of the neuroendocrine axis to the cellular response.