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The Androgen Receptor Antagonizes Wnt/β-Catenin Signaling in Epidermal Stem Cells

Kai Kretzschmar1, Denny L Cottle2, Pawel J Schweiger3

  • 1Centre for Stem Cells and Regenerative Medicine, King's College London, Guy's Hospital Campus, London, UK; Wellcome Trust-Medical Research Council Stem Cell Institute, University of Cambridge, Cambridge, UK.

The Journal of Investigative Dermatology
|June 30, 2015
PubMed

Insights

Androgen receptor (AR) signaling modulates Wnt/β-catenin pathways in mouse skin. AR activation blocks hair follicle growth and sebaceous gland conversion, while AR inhibition promotes these effects, impacting stem cell fate.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Stem Cell Biology

Background:

  • Wnt/β-catenin signaling drives stem cell expansion and hair follicle (HF) differentiation in mouse epidermis.
  • Sebaceous glands (SGs) can be redirected to differentiate along HF lineages upon Wnt/β-catenin activation.

Purpose of the Study:

  • To investigate the reciprocal interaction between androgen receptor (AR) and β-catenin signaling during epidermal development and homeostasis.
  • To determine the role of AR in modulating β-catenin-driven stem cell fate selection in adult mouse skin.

Main Methods:

  • Utilized mouse models to study epidermal development and homeostasis.
  • Manipulated Wnt/β-catenin and AR signaling pathways.
  • Analyzed effects on keratinocyte differentiation, HF growth, and SG identity.

Main Results:

  • Reciprocal activation of AR and β-catenin observed in HF bulb cells.
  • AR activation suppressed β-catenin-dependent transcription and blocked HF growth and SG conversion.
  • AR inhibition enhanced β-catenin effects, leading to HF proliferation, differentiation, benign HF tumors, and loss of SG identity.

Conclusions:

  • AR signaling plays a crucial role in epidermal stem cell fate selection.
  • AR modulates cellular responses to β-catenin in adult mouse skin, influencing HF and SG development.

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