Endothelial Cell Activation Is Regulated ...
Type de document :
Article dans une revue scientifique: Article original
DOI :
PMID :
Titre :
Endothelial Cell Activation Is Regulated by Epidermal Growth Factor-like Domain 7 (Egfl7) during Inflammation
Auteur(s) :
Pinte, Sébastien [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Caetano, Bertrand [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Le Bras, Alexandra [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Havet, Chantal [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Villain, Gaëlle [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Dernayka, Racha [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Duez, Catherine [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Mattot, Virginie [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Soncin, Fabrice [Auteur correspondant]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Caetano, Bertrand [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Le Bras, Alexandra [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Havet, Chantal [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Villain, Gaëlle [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Dernayka, Racha [Auteur]
Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Duez, Catherine [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Mattot, Virginie [Auteur]

Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Soncin, Fabrice [Auteur correspondant]

Mécanismes de la Tumorigénèse et Thérapies Ciblées - UMR 8161 [M3T]
Titre de la revue :
Journal of Biological Chemistry
Pagination :
24017-24028
Éditeur :
American Society for Biochemistry and Molecular Biology
Date de publication :
2016-11
ISSN :
0021-9258
Mot(s)-clé(s) en anglais :
NF-kappa B (NF-KB)
adhesion
endothelium
inflammation
leukocyte
vascular biology
adhesion
endothelium
inflammation
leukocyte
vascular biology
Discipline(s) HAL :
Sciences du Vivant [q-bio]/Biologie cellulaire/Interactions cellulaires [q-bio.CB]
Résumé en anglais : [en]
Activation of the blood vessel endothelium is a critical step during inflammation. Endothelial cells stimulated by pro-inflammatory cytokines play an essential part in the adhesion and extravasation of circulating leukocytes ...
Lire la suite >Activation of the blood vessel endothelium is a critical step during inflammation. Endothelial cells stimulated by pro-inflammatory cytokines play an essential part in the adhesion and extravasation of circulating leukocytes into inflamed tissues. The endothelial egfl7 gene (VE-statin) represses endothelial cell activation in tumors, and prior observations suggested that it could also participate in the regulation of endothelial cell activation during inflammation. We show here that Egfl7 expression is strongly repressed in mouse lung endothelial cells during LPS- and TNFα-induced inflammation in vivo LPS have a limited effect on Egfl7 expression by endothelial cells in vitro, whereas the pro-inflammatory cytokine TNFα strongly represses Egfl7 expression in endothelial cells. TNFα regulates the egfl7 gene promoter through regions located between -7585 and -5550 bp ahead of the main transcription start site and via an NF-κB-dependent mechanism. Conversely, Egfl7 regulates the response of endothelial cells to TNFα by restraining the induced expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin, resulting in a decreased adhesion of leukocytes onto endothelial cells stimulated by TNFα. Egfl7 regulates the expression of these adhesion molecules through the NF-κB and MEK/Erk pathways, in particular by preventing the proteasome-mediated degradation of IkBα both in non-activated endothelial cells and during activation. Egfl7 is thus an endogenous and constitutive repressor of blood vessel endothelial cell activation in normal and inflammatory conditions and participates in a loop of regulation of activation of these cells by pro-inflammatory cytokines.Lire moins >
Lire la suite >Activation of the blood vessel endothelium is a critical step during inflammation. Endothelial cells stimulated by pro-inflammatory cytokines play an essential part in the adhesion and extravasation of circulating leukocytes into inflamed tissues. The endothelial egfl7 gene (VE-statin) represses endothelial cell activation in tumors, and prior observations suggested that it could also participate in the regulation of endothelial cell activation during inflammation. We show here that Egfl7 expression is strongly repressed in mouse lung endothelial cells during LPS- and TNFα-induced inflammation in vivo LPS have a limited effect on Egfl7 expression by endothelial cells in vitro, whereas the pro-inflammatory cytokine TNFα strongly represses Egfl7 expression in endothelial cells. TNFα regulates the egfl7 gene promoter through regions located between -7585 and -5550 bp ahead of the main transcription start site and via an NF-κB-dependent mechanism. Conversely, Egfl7 regulates the response of endothelial cells to TNFα by restraining the induced expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin, resulting in a decreased adhesion of leukocytes onto endothelial cells stimulated by TNFα. Egfl7 regulates the expression of these adhesion molecules through the NF-κB and MEK/Erk pathways, in particular by preventing the proteasome-mediated degradation of IkBα both in non-activated endothelial cells and during activation. Egfl7 is thus an endogenous and constitutive repressor of blood vessel endothelial cell activation in normal and inflammatory conditions and participates in a loop of regulation of activation of these cells by pro-inflammatory cytokines.Lire moins >
Langue :
Anglais
Comité de lecture :
Oui
Audience :
Internationale
Vulgarisation :
Non
Source :
Fichiers
- https://www.hal.inserm.fr/inserm-03809989/document
- Accès libre
- Accéder au document
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5104927/pdf
- Accès libre
- Accéder au document
- document
- Accès libre
- Accéder au document
- J.%20Biol.%20Chem.-2016-Pinte-24017-28.pdf
- Accès libre
- Accéder au document
- Accès libre
- Accéder au document
- document
- Accès libre
- Accéder au document
- J.%20Biol.%20Chem.-2016-Pinte-24017-28.pdf
- Accès libre
- Accéder au document
- document
- Accès libre
- Accéder au document
- J.%20Biol.%20Chem.-2016-Pinte-24017-28.pdf
- Accès libre
- Accéder au document