PuSH - Publication Server of Helmholtz Zentrum München: Targeting activation of specific NF-κB subunits prevents stress-dependent atherothrombotic gene expression.

Information

Clues to quality of journals

Open Access Policy of Helmholtz Association 2016

CC Licencences

Publication Metrics

Navigation

Home

Deutsch

EVA: Electronic Publishing

New EVA Application

Research

Advanced Search

Browse by ...

... HMGU-Authors/Consortia

... Organizational Structure

... Journal

... Publication Type

... Research Data

... Arbeitsgruppen

... Publication Year

Publication overview

Statistics

Statistics (last 5 years)

OA Publications

Publish

Submit Publication

Import publication from...

...EVA

Report missing publication

Highlights

Support & Contact

Contact persons

Help

Data protection

Helmholtz Open Science

JANE Journal Estimator

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Djuric, Z.* ; Kashif, M.* ; Fleming, T.* ; Muhammad, S.* ; Piel, D.* ; von Bauer, R.* ; Bea, F.* ; Herzig, S.* ; Zeier, M.* ; Pizzi, M.* ; Isermann, B.* ; Hecker, M.* ; Schwaninger, M.* ; Bierhaus, A.* ; Nawroth, P.P.*

Targeting activation of specific NF-κB subunits prevents stress-dependent atherothrombotic gene expression.

Mol. Med. 18, 1375-1386 (2012)

DOI

PMC

Open Access Gold as soon as Publ. Version/Full Text is submitted to ZB.

Abstract
Metrics
Extra information

Psychosocial stress has been shown to be a contributing factor in the development of atherosclerosis. Although the underlying mechanisms have not been elucidated entirely, it has been shown previously that the transcription factor nuclear factor-κB (NF-κB) is an important component of stress-activated signaling pathway. In this study, we aimed to decipher the mechanisms of stress-induced NF-κB-mediated gene expression, using an in vitro and in vivo model of psychosocial stress. Induction of stress led to NF-κB-dependent expression of proinflammatory (tissue factor, intracellular adhesive molecule 1 [ICAM-1]) and protective genes (manganese superoxide dismutase [MnSOD]) via p50, p65 or cRel. Selective inhibition of the different subunits and the respective kinases showed that inhibition of cRel leads to the reduction of atherosclerotic lesions in apolipoprotein(-/-) (ApoE(-/-)) mice via suppression of proinflammatory gene expression. This observation may therefore provide a possible explanation for ineffectiveness of antioxidant therapies and suggests that selective targeting of cRel activation may provide a novel approach for the treatment of stress-related inflammatory vascular disease.

Impact Factor

Scopus SNIP

Web of Science
Times Cited

Altmetric

0.000

1.608