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

Christopher Scott, James Bonner, Danqing Min, Philip Boughton, Rebecca Stokes, Kuan Minn Cha, Stacey N. Walters, Kendle Maslowski, Frederic Sierro, Shane T. Grey, Stephen Twigg, Susan McLennan, Jenny E. Gunton

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)C349-C357
Number of pages9
JournalAmerican Journal of Physiology - Cell Physiology
Issue number4
Publication statusPublished - 15 Aug 2014


  • Aryl hydrocarbon receptor nuclear translocator
  • Deferoxamine
  • Hypoxia-inducible factor-1α

ASJC Scopus subject areas

  • Physiology
  • Cell Biology


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