Changes in expression of apoptosis-associated genes in skin mark early catagen

J Invest Dermatol. 1995 Jan;104(1):78-82. doi: 10.1111/1523-1747.ep12613555.

Abstract

Programmed cell death is central to hair biology, as the hair follicle undergoes cycles of growth (anagen), regression (catagen), and rest (telogen). During catagen, the hair follicle shortens via a pathway of programmed cell death and apoptosis. The molecular mechanisms involved in this process have not been elucidated yet. Using reverse transcriptase-polymerase chain reaction, we examined in this study the expression in total skin, throughout one hair cycle, of a series of regulatory genes associated with apoptosis. We show that gene expression within skin is hair-cycle-dependent. Transforming growth factor-beta was expressed immediately before catagen; therefore, it might be involved in the early signaling of this process. Tumor necrosis factor-beta was expressed during catagen and might be involved in follicular apoptosis. Several proto-oncogenes and transcription factors have been described in the regulation of apoptosis in other systems. Here we show that the transcript levels of c-myc, c-myb, and c-jun changed immediately before or during early catagen and thus could be involved in the signaling or regulation of catagen. Levels of p53 remained constant throughout anagen and catagen, suggesting that p53 is not involved in the developmentally induced apoptosis of the hair follicle. The variable expression throughout the hair cycle of the genes described demonstrates the dynamic changes of the skin and underscores the importance of studying the complete hair cycle when characterizing any molecule in skin.

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Base Sequence
  • Cell Division / physiology
  • Female
  • Gene Expression / physiology
  • Hair / cytology
  • Lymphotoxin-alpha / physiology
  • Mice
  • Mice, Inbred Strains
  • Molecular Sequence Data
  • Polymerase Chain Reaction / methods
  • Skin / cytology*
  • Transcription Factors / physiology
  • Transforming Growth Factor beta / physiology
  • Tumor Necrosis Factor-alpha / physiology

Substances

  • Lymphotoxin-alpha
  • Transcription Factors
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha