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

Details

Serval ID
serval:BIB_D88237A93D2D
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Reduction of ARNT in myeloid cells causes immune suppression and delayed wound healing.
Journal
American Journal of Physiology. Cell Physiology
Author(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
Publication state
Published
Issued date
2014
Volume
307
Number
4
Pages
C349-C357
Language
english
Abstract
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.
Keywords
aryl hydrocarbon receptor nuclear translocator, hypoxia-inducible factor-1 alpha, deferoxamine
Pubmed
Web of science
Create date
26/09/2014 8:24
Last modification date
20/08/2019 15:58
Usage data