The effect of ultraviolet B induced adult T cell leukemia-derived factor/thioredoxin (ADF/TRX) on survival and growth of human melanocytes

Pigment Cell Res. 1997 Feb-Apr;10(1-2):68-73. doi: 10.1111/j.1600-0749.1997.tb00469.x.

Abstract

Ultraviolet B (UVB) radiation is known to induce reactive oxygen species (ROS) in the skin. The skin, however, counteracts ROS by both constitutional and newly produced antioxidants. One such antioxidant, adult T cell leukemia-derived factor (ADF), a human homologue of thioredoxin (TRX), was shown to be efficiently produced in and released from cultured normal human keratinocytes after UVB irradiation by Northern and Western blot analyses and enzyme-linked immunoabsorbent assay (ELISA). Recombinant ADF (rADF) did not rescue UVB-induced melanocyte death, either when added pre- or post-UV irradiation. However, further addition of neutralizing antibody caused cell death of both keratinocytes and melanocytes. rADF was shown to induce higher expression in melanocortin-1 receptor (MC1-R) mRNA accompanied by increased binding activity using 125I labeled [Nle4, D-Phe7]-alpha-MSH in melanocytes, leading to the enhanced increment of DNA synthesis. Taken together, it was shown that released ADF from UVB-irradiated keratinocytes acts as a survival factor for both keratinocytes and melanocytes but does not rescue UV-induced melanocyte death. Further, it may work as one of the stimulatory factors for UVB-induced melanogenesis by upregulating MSH-R binding activity in combination with the enhanced DNA synthesis by alpha-MSH.

MeSH terms

  • Adolescent
  • Adult
  • Cell Division / drug effects
  • Cell Survival / drug effects
  • Cells, Cultured
  • Cytokines / biosynthesis
  • Cytokines / pharmacology*
  • DNA / biosynthesis
  • Growth Substances / biosynthesis
  • Growth Substances / pharmacology*
  • Humans
  • Male
  • Melanocytes / cytology
  • Melanocytes / drug effects*
  • Melanocytes / metabolism
  • Melanocytes / radiation effects*
  • Neoplasm Proteins / biosynthesis
  • Neoplasm Proteins / pharmacology*
  • Receptors, Pituitary Hormone / genetics
  • Receptors, Pituitary Hormone / metabolism
  • Recombinant Proteins / pharmacology
  • Thioredoxins / biosynthesis
  • Thioredoxins / pharmacology*
  • Ultraviolet Rays*

Substances

  • Cytokines
  • Growth Substances
  • Neoplasm Proteins
  • Receptors, Pituitary Hormone
  • Recombinant Proteins
  • adult T cell leukemia-derived factor
  • Thioredoxins
  • MSH receptor
  • DNA