Estrogen receptor-mediated signalling in female mice is locally activated in response to wounding.

Détails

ID Serval
serval:BIB_BAE0242C78BA
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Estrogen receptor-mediated signalling in female mice is locally activated in response to wounding.
Périodique
Molecular and Cellular Endocrinology
Auteur⸱e⸱s
Emmerson E., Rando G., Meda C., Campbell L., Maggi A., Hardman M.J.
ISSN
1872-8057 (Electronic)
ISSN-L
0303-7207
Statut éditorial
Publié
Date de publication
2013
Volume
375
Numéro
1-2
Pages
149-156
Langue
anglais
Résumé
Estrogen deprivation is associated with delayed healing, while Hormone Replacement Therapy (HRT) accelerates acute wound healing and protects against development of chronic wounds. Estrogen exerts its effects on healing via numerous cell types by signalling through the receptors ERα and ERβ, which bind to the Estrogen Responsive Element (ERE) and initiate gene transcription. The ERE-luciferase transgenic mouse model has been influential in assessing real-time in vivo estrogen receptor activation across a range of tissues and pathologies. Using this model we demonstrate novel temporally regulated peri-wound activation of estrogen signalling in female mice. Using histological methods we reveal that this signal is specifically localised to keratinocytes of the neoepidermis and wound margin dermal cells. Moreover using pharmacological agonists we reveal that ERβ induces ERE-mediated signal in both epidermal and dermal cells while ERα induces ERE-mediated signal in dermal cells alone. Collectively these novel data demonstrate rapid and regional activation of estrogen signalling in wounded skin. A more complete understanding of local hormonal signalling during repair is essential for the focussed development of new therapies for wound healing.
Mots-clé
Estrogen, Wound healing, Estrogen receptors, ERE, Skin, Luciferase
Pubmed
Web of science
Création de la notice
02/09/2013 9:54
Dernière modification de la notice
20/08/2019 16:28
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