Egr1 deficiency induces browning of inguinal subcutaneous white adipose tissue in mice - Evolution Paris Seine Accéder directement au contenu
Article Dans Une Revue Scientific Reports Année : 2017

Egr1 deficiency induces browning of inguinal subcutaneous white adipose tissue in mice

Résumé

Abstract Beige adipocyte differentiation within white adipose tissue, referred to as browning, is seen as a possible mechanism for increasing energy expenditure. The molecular regulation underlying the thermogenic browning process has not been entirely elucidated. Here, we identify the zinc finger transcription factor EGR1 as a negative regulator of the beige fat program. Loss of Egr1 in mice promotes browning in the absence of external stimulation and leads to an increase of Ucp1 expression, which encodes the key thermogenic mitochondrial uncoupling protein-1. Moreover, EGR1 is recruited to the proximal region of the Ucp1 promoter in subcutaneous inguinal white adipose tissue. Transcriptomic analysis of subcutaneous inguinal white adipose tissue in the absence of Egr1 identifies the molecular signature of white adipocyte browning downstream of Egr1 deletion and highlights a concomitant increase of beige differentiation marker and a decrease in extracellular matrix gene expression. Conversely, Egr1 overexpression in mesenchymal stem cells decreases beige adipocyte differentiation, while increasing extracellular matrix production. These results reveal a role for Egr1 in blocking energy expenditure via direct Ucp1 transcription repression and highlight Egr1 as a therapeutic target for counteracting obesity.
Fichier principal
Vignette du fichier
2017 Scientific Reports Manu.pdf (8.88 Mo) Télécharger le fichier
Origine : Fichiers éditeurs autorisés sur une archive ouverte

Dates et versions

hal-03991213 , version 1 (15-02-2023)

Identifiants

Citer

Cécile Milet, Marianne Bléher, Kassandra Allbright, Mickael Orgeur, Fanny Coulpier, et al.. Egr1 deficiency induces browning of inguinal subcutaneous white adipose tissue in mice. Scientific Reports, 2017, 7 (1), pp.16153. ⟨10.1038/s41598-017-16543-7⟩. ⟨hal-03991213⟩
15 Consultations
0 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More