Influence of genistein on c-Jun, c-Fos and Fos-B of AP-1 subunits expression in skin keratinocytes, fibroblasts and keloid fibroblasts cultured in vitro

Acta Pol Pharm. 2013 Mar-Apr;70(2):205-13.

Abstract

Genistein is a well known flavonoid that exhibits antioxidant, antiproliferative, proapoptotic, antiangiogenic, as well as estrogenic and anti-estrogenic activity. Extensive studies in the field of dermatology and cosmetology in recent years revealed that genistein is a promising anti-aging, anti-photoaging and anti-carcinogenic agent for skin care. Essential role in skin prematuring aging and carcinogenesis play AP-1 transcription factors that are activated, among others, by environmental factors: ultraviolet light and free radicals. Genistein is a potent antioxidant and inhibitor of AP-1 activity. The aim of the study was to investigate genistein as a potential regulator of C-JUN, C-FOS and FOS-B of AP-1 subunits expression in skin keratinocytes, fibroblasts and keloid fibroblasts cultured in vitro. In presented study, genistein modulated C-JUN expression in epidermal keratinocytes and dermal fibroblasts cultured in vitro. The expression of C-JUN was higher in keratinocytes treated with 37 and 370 microM genistein. In dermal fibroblasts genistein regulated C-JUN expression in dose-dependent manner. The expression of C-JUN was lower in fibroblasts treated with 370 microM genistein and higher in fibroblasts treated with 37 microM genistein. Genistein in 370 microM concentration inhibited C-FOS expression in fibroblasts, whereas in 370 and 37 microM concentration genistein inhibited FOS-B expression in keratinocytes. Furthermore, genistein was able to modulate C-JUN and C-FOS genes expression in keloid fibroblasts cultured in vitro. In these cells, transcriptional activity of C-JUN and C-FOS expression depended on employed concentration of genistein. The expression of C-JUN and C-FOS was higher in keloid fibroblasts treated with 370 microM genistein and lower in keloid fibroblasts treated with 37 microM genistein.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Cell Survival / drug effects
  • Dermatologic Agents / pharmacology*
  • Dose-Response Relationship, Drug
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Gene Expression Regulation
  • Genistein / pharmacology*
  • Humans
  • Keloid / metabolism
  • Keloid / pathology*
  • Keratinocytes / drug effects*
  • Keratinocytes / metabolism
  • Proto-Oncogene Proteins c-fos / genetics
  • Proto-Oncogene Proteins c-fos / metabolism*
  • Proto-Oncogene Proteins c-jun / genetics
  • Proto-Oncogene Proteins c-jun / metabolism*
  • RNA, Messenger / metabolism
  • Transcription Factor AP-1 / genetics
  • Transcription Factor AP-1 / metabolism*

Substances

  • Dermatologic Agents
  • FOSB protein, human
  • Proto-Oncogene Proteins c-fos
  • Proto-Oncogene Proteins c-jun
  • RNA, Messenger
  • Transcription Factor AP-1
  • Genistein