Focal adhesion kinase modulates activation of NF-kappaB by flow in endothelial cells.
Am J Physiol Cell Physiol
; 297(4): C814-22, 2009 Oct.
Article
em En
| MEDLINE
| ID: mdl-19587216
ABSTRACT
Atherogenesis involves activation of NF-kappaB in endothelial cells by fluid shear stress. Because this pathway involves integrins, we investigated the involvement of focal adhesion kinase (FAK). We found that FAK was not required for flow-stimulated translocation of the p65 NF-kappaB subunit to the nucleus but was essential for phosphorylation of p65 on serine 536 and induction of ICAM-1, an NF-kappaB-dependent gene. NF-kappaB activation by TNF-alpha or hydrogen peroxide was FAK independent. Events upstream of NF-kappaB, including integrin activation, Rac activation, reactive oxygen production, and degradation of IkappaB, were FAK independent. FAK therefore regulates NF-kappaB phosphorylation and transcriptional activity in response to flow by a novel mechanism.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Endotélio Vascular
/
NF-kappa B
/
Células Endoteliais
/
Proteína-Tirosina Quinases de Adesão Focal
Idioma:
En
Ano de publicação:
2009
Tipo de documento:
Article