TNF up-regulates ST3GAL4 and sialyl-Lewisx ...
Type de document :
Article dans une revue scientifique
DOI :
URL permanente :
Titre :
TNF up-regulates ST3GAL4 and sialyl-Lewisx expression in lung epithelial cells through an intronic ATF2-responsive element
Auteur(s) :
Colomb, Florent [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Krzewinski, Marie-Ange [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Steenackers, Agata [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle - UMR 8576 [UGSF]
Vincent, Audrey [Auteur]
Harduin Lepers, Anne [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Delannoy, Philippe [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Groux, Sophie [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Krzewinski, Marie-Ange [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Steenackers, Agata [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle - UMR 8576 [UGSF]
Vincent, Audrey [Auteur]
Harduin Lepers, Anne [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Delannoy, Philippe [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Groux, Sophie [Auteur]
Unité de Glycobiologie Structurale et Fonctionnelle UMR 8576 [UGSF]
Titre de la revue :
The Biochemical Journal
Nom court de la revue :
Biochem J
Numéro :
474
Pagination :
65-78
Date de publication :
2017-01-01
ISSN :
0264-6021, 1470-8728
Mot(s)-clé(s) en anglais :
A549 Cells
ATF2
Response Elements
Humans
Oligosaccharide
intronic element
Lung
Respiratory Mucosa
Epithelial Cells
Inflammation
Sialyltransferase
Extracellular Signal-Regulated MAP Kinases
Transcriptional regulation
Tumor Necrosis Factor-alpha
MAP Kinase Signaling System
Activating Transcription Factor 2
Pseudomonas aeruginosa
Proto-Oncogene Protein c-ets-1
ATF2
Response Elements
Humans
Oligosaccharide
intronic element
Lung
Respiratory Mucosa
Epithelial Cells
Inflammation
Sialyltransferase
Extracellular Signal-Regulated MAP Kinases
Transcriptional regulation
Tumor Necrosis Factor-alpha
MAP Kinase Signaling System
Activating Transcription Factor 2
Pseudomonas aeruginosa
Proto-Oncogene Protein c-ets-1
Discipline(s) HAL :
Chimie/Chimie théorique et/ou physique
Résumé en anglais : [en]
We have previously shown that tumor necrosis factor (TNF) induced the up-regulation of the sialyltransferase gene ST3GAL4 (α2,3-sialyltransferase gene) BX transcript through mitogen- and stress-activated kinase 1/2 (MSK1/2), ...
Lire la suite >We have previously shown that tumor necrosis factor (TNF) induced the up-regulation of the sialyltransferase gene ST3GAL4 (α2,3-sialyltransferase gene) BX transcript through mitogen- and stress-activated kinase 1/2 (MSK1/2), extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) signaling pathways. This up-regulation resulted in sialyl-Lewisx (sLex) overexpression on high-molecular-weight glycoproteins in inflamed airway epithelium and increased the adhesion of Pseudomonas aeruginosa PAO1 and PAK strains to lung epithelial cells. In the present study, we describe a TNF-responsive element in an intronic region of the ST3GAL4 gene, whose TNF-dependent activity is repressed by ERK/p38 and MSK1/2 inhibitors. This TNF-responsive element contains potential binding sites for ETS1 and ATF2 transcription factors related to TNF signaling. We also show that ATF2 is involved in TNF responsiveness, as well as in TNF-induced ST3GAL4 BX transcript and sLex overexpression in A549 lung epithelial cells. Moreover, we show that TNF induces the binding of ATF2 to the TNF-responsive element. Altogether, these data suggest that ATF2 could be a potential target to prevent inflammation-induced P. aeruginosa binding in the lung of patients suffering from lung diseases such as chronic bronchitis or cystic fibrosis.Lire moins >
Lire la suite >We have previously shown that tumor necrosis factor (TNF) induced the up-regulation of the sialyltransferase gene ST3GAL4 (α2,3-sialyltransferase gene) BX transcript through mitogen- and stress-activated kinase 1/2 (MSK1/2), extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) signaling pathways. This up-regulation resulted in sialyl-Lewisx (sLex) overexpression on high-molecular-weight glycoproteins in inflamed airway epithelium and increased the adhesion of Pseudomonas aeruginosa PAO1 and PAK strains to lung epithelial cells. In the present study, we describe a TNF-responsive element in an intronic region of the ST3GAL4 gene, whose TNF-dependent activity is repressed by ERK/p38 and MSK1/2 inhibitors. This TNF-responsive element contains potential binding sites for ETS1 and ATF2 transcription factors related to TNF signaling. We also show that ATF2 is involved in TNF responsiveness, as well as in TNF-induced ST3GAL4 BX transcript and sLex overexpression in A549 lung epithelial cells. Moreover, we show that TNF induces the binding of ATF2 to the TNF-responsive element. Altogether, these data suggest that ATF2 could be a potential target to prevent inflammation-induced P. aeruginosa binding in the lung of patients suffering from lung diseases such as chronic bronchitis or cystic fibrosis.Lire moins >
Langue :
Anglais
Audience :
Non spécifiée
Établissement(s) :
CNRS
Université de Lille
Université de Lille
Équipe(s) de recherche :
Régulation de la glycosylation terminale
Mécanismes moléculaires de la N-glycosylation et pathologies associées
Mécanismes moléculaires de la N-glycosylation et pathologies associées
Date de dépôt :
2020-02-12T15:44:40Z
2021-02-25T09:29:37Z
2021-06-28T07:55:13Z
2021-02-25T09:29:37Z
2021-06-28T07:55:13Z