The expression of endothelin-1 and its binding sites in mouse skin increased after ultraviolet B irradiation or local injection of tumor necrosis factor alpha

J Dermatol. 1998 Feb;25(2):78-84. doi: 10.1111/j.1346-8138.1998.tb02354.x.


Endothelin (ET)-1 is a 21-amino acid peptide which has vasoconstrictor and growth regulatory activity. Recently, cultured keratinocytes have been reported to express ET-1 and its receptor when irradiated by ultraviolet (UV) B. In order to further understand the role of ET-1 in vivo during UVB-induced inflammation, we examined the localization, intensity and time course of the expression levels of ET-1 and its binding sites in UVB-exposed BALB/c mouse skin. Frozen and paraffin sections prepared from mouse skin 48 h after treatment with UVB irradiation (0.36 or 0.72 J/cm2) or after injection with tumor necrosis factor (TNF)-alpha (1.0 microgram) or interleukin (IL)-1 alpha (0.05 microgram) were incubated with monoclonal anti-ET-1 IgG and then visualized by peroxidase staining. In normal skin, faint ET-1 immunoreactivity was observed in the epidermis, pilosebaceous structures and blood vessels. Upon exposure to UVB irradiation or administration of TNF-alpha injection or IL-1 alpha injection, such immunoreactivity was found to be significantly enhanced. Subsequently, the frozen sections were incubated with 125I ET-1 for 30 min, and visualized by autoradiographic technique. In normal skin, ET-1 weakly bound to the skin, while UVB irradiation and TNF-alpha injection significantly enhanced ET-1 binding in the epidermis, pilosebaceous structures and blood vessels. Time course experiments (1, 2, 4 and 7 days) indicated that ET-1 immunoreactivity and ET-1 binding peaked 1 or 2 days after UVB irradiation or TNF-alpha injection. These results suggest that the up-regulated expression of ET-1 and its binding sites in the epidermis and pilosebaceous structures may act as an autocrine/paracrine factor during UVB-induced inflammation.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Binding Sites
  • Culture Techniques
  • Disease Models, Animal
  • Endothelin-1 / analysis*
  • Immunohistochemistry
  • Injections, Intradermal
  • Keratinocytes / drug effects*
  • Keratinocytes / metabolism
  • Keratinocytes / radiation effects*
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Reference Values
  • Skin / chemistry*
  • Skin / drug effects
  • Skin / metabolism
  • Skin / radiation effects
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Ultraviolet Rays*


  • Endothelin-1
  • Tumor Necrosis Factor-alpha