Inflammatory murine skin responses to UV-B light are partially dependent on endothelin-1 and mast cells

Am J Pathol. 2006 Sep;169(3):815-22. doi: 10.2353/ajpath.2006.060037.

Abstract

Endothelin (ET-1) has been shown to crucially contribute to UV-induced skin responses such as tanning. To test whether ET-1 is also involved in early cutaneous reactions to UV, we assessed ET-1 skin levels in UV-irradiated mice. In correlation with the levels of UV-induced skin inflammation, ET-1 concentrations increased substantially and continually. Moreover, blocking of ET-1 receptors (ETA) resulted in significantly decreased cutaneous inflammation following UV irradiation. When we assessed skin responses to ET-1 injections, we observed prominent mast cell degranulation and mast cell-dependent inflammation. Since mast cells also critically contributed to UV-induced inflammation, we determined the ET-1-dependent inflammatory response to UV in the absence and presence of these cells. Interestingly, ETA blockade did not decrease UV-induced inflammation in mast cell-deficient mice, unless these mice had been adoptively transferred with mast cells before irradiation. This indicates that skin inflammation due to UV irradiation is caused in part by ET-1 acting on skin mast cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Degranulation / genetics
  • Cell Degranulation / radiation effects*
  • Dermatitis / metabolism*
  • Dermatitis / pathology
  • Dose-Response Relationship, Radiation
  • Endothelin A Receptor Antagonists
  • Endothelin-1 / metabolism*
  • Inflammation / genetics
  • Inflammation / metabolism
  • Inflammation / pathology
  • Mast Cells / metabolism*
  • Mast Cells / pathology
  • Mice
  • Mice, Transgenic
  • Receptor, Endothelin A / metabolism*
  • Ultraviolet Rays / adverse effects*

Substances

  • Endothelin A Receptor Antagonists
  • Endothelin-1
  • Receptor, Endothelin A