Plasminogen activation is required for the development of radiation-induced dermatitis

Cell Death Dis. 2018 Oct 15;9(11):1051. doi: 10.1038/s41419-018-1106-8.

Abstract

Skin damage caused by radiation therapy (radiodermatitis) is a severe side effect of radiotherapy in cancer patients, and there is currently a lack of effective strategies to prevent or treat such skin damage. In this work, we show with several lines of evidence that plasminogen, a pro-inflammatory factor, is key for the development of radiodermatitis. After skin irradiation in wild-type (plg+/+) mice, the plasminogen level increased in the irradiated area, leading to severe skin damage such as ulcer formation. However, plasminogen-deficient (plg-/-) mice and mice lacking plasminogen activators were mostly resistant to radiodermatitis. Moreover, treatment with a plasminogen inhibitor, tranexamic acid, decreased radiodermatitis in plg+/+ mice and prevented radiodermatitis in plg+/- mice. Together with studies at the molecular level, we report that plasmin is required for the induction of inflammation after irradiation that leads to radiodermatitis, and we propose that inhibition of plasminogen activation can be a novel treatment strategy to reduce and prevent the occurrence of radiodermatitis in patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Movement / drug effects
  • Disease Models, Animal
  • Enzyme Inhibitors / pharmacology*
  • Gene Expression Regulation
  • Heterozygote
  • Homozygote
  • Humans
  • Interleukin-1beta / genetics
  • Interleukin-1beta / immunology
  • Macrophages / drug effects
  • Macrophages / immunology
  • Macrophages / pathology
  • Macrophages / radiation effects
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Neutrophils / drug effects
  • Neutrophils / immunology
  • Neutrophils / pathology
  • Neutrophils / radiation effects
  • Plasminogen / antagonists & inhibitors
  • Plasminogen / genetics*
  • Plasminogen / immunology
  • Plasminogen Activator Inhibitor 1 / agonists
  • Plasminogen Activator Inhibitor 1 / genetics
  • Plasminogen Activator Inhibitor 1 / immunology
  • Plasminogen Activators / antagonists & inhibitors
  • Plasminogen Activators / genetics*
  • Plasminogen Activators / immunology
  • Radiation-Protective Agents / pharmacology*
  • Radiodermatitis / genetics
  • Radiodermatitis / immunology
  • Radiodermatitis / pathology
  • Radiodermatitis / prevention & control*
  • Signal Transduction
  • Skin / drug effects
  • Skin / immunology
  • Skin / pathology
  • Skin / radiation effects
  • Tranexamic Acid / pharmacology*
  • Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta / immunology
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology

Substances

  • Enzyme Inhibitors
  • IL1B protein, mouse
  • Interleukin-1beta
  • Plasminogen Activator Inhibitor 1
  • Radiation-Protective Agents
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • Tranexamic Acid
  • Plasminogen
  • Plasminogen Activators