Reduction of ARNT in myeloid cells causes immune suppression and delayed wound healing.

Détails

ID Serval
serval:BIB_D88237A93D2D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Reduction of ARNT in myeloid cells causes immune suppression and delayed wound healing.
Périodique
American Journal of Physiology. Cell Physiology
Auteur⸱e⸱s
Scott C., Bonner J., Min D., Boughton P., Stokes R., Cha K.M., Walters S.N., Maslowski K., Sierro F., Grey S.T., Twigg S., McLennan S., Gunton J.E.
ISSN
1522-1563 (Electronic)
ISSN-L
0363-6143
Statut éditorial
Publié
Date de publication
2014
Volume
307
Numéro
4
Pages
C349-C357
Langue
anglais
Résumé
Aryl hydrocarbon receptor nuclear translocator (ARNT) is a transcription factor that binds to partners to mediate responses to environmental signals. To investigate its role in the innate immune system, floxed ARNT mice were bred with lysozyme M-Cre recombinase animals to generate lysozyme M-ARNT (LAR) mice with reduced ARNT expression. Myeloid cells of LAR mice had altered mRNA expression and delayed wound healing. Interestingly, when the animals were rendered diabetic, the difference in wound healing between the LAR mice and their littermate controls was no longer present, suggesting that decreased myeloid cell ARNT function may be an important factor in impaired wound healing in diabetes. Deferoxamine (DFO) improves wound healing by increasing hypoxia-inducible factors, which require ARNT for function. DFO was not effective in wounds of LAR mice, again suggesting that myeloid cells are important for normal wound healing and for the full benefit of DFO. These findings suggest that myeloid ARNT is important for immune function and wound healing. Increasing ARNT and, more specifically, myeloid ARNT may be a therapeutic strategy to improve wound healing.
Mots-clé
aryl hydrocarbon receptor nuclear translocator, hypoxia-inducible factor-1 alpha, deferoxamine
Pubmed
Web of science
Création de la notice
26/09/2014 9:24
Dernière modification de la notice
20/08/2019 16:58
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