The ion channel, TRPM2, contributes to the pathogenesis of radiodermatitis

Anne Laure Perraud, Deviyani M. Rao, Elizabeth A. Kosmacek, Aleksandra Dagunts, Rebecca E. Oberley-Deegan, Fabienne Gally

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

Radiodermatitis is a painful side effect for cancer patients undergoing radiotherapy. Irradiation of the skin causes inflammation and breakdown of the epidermis and can lead to significant morbidity and mortality in severe cases, as seen in exposure from accidents or weapons such as “dirty bombs” and ultimately leads to tissue fibrosis. However, the pathogenesis of radiodermatitis is not fully understood. Using a mouse model of radiodermatitis, we showed that the Transient Receptor Potential Melastatin 2 (TRPM2) ion channel plays a significant role in the development of dermatitis following exposure to ionizing radiation. Irradiated TRPM2-deficient mice developed less inflammation, fewer severe skin lesions and decreased fibrosis when compared to wild type mice. The TRPM2-deficient mice also showed a faster recovery period as seen by their increased weight gain post irradiation. Finally, TRPM2-deficient mice exhibited lower systemic inflammation with a reduction in inflammatory cytokines present in the serum. These findings suggest that TRPM2 may be a potential therapeutic target for reducing the severity of radiodermatitis.

Original languageEnglish (US)
Pages (from-to)89-98
Number of pages10
JournalRadiation and Environmental Biophysics
Volume58
Issue number1
DOIs
StatePublished - Mar 8 2019

Keywords

  • Inflammation
  • Mouse
  • Radiodermatitis
  • Transient receptor potential channels (TRP channels)
  • Trpm2

ASJC Scopus subject areas

  • Biophysics
  • Radiation
  • Environmental Science(all)

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