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Structural and biochemical changes underlying a keratoderma-like phenotype in mice lacking suprabasal AP1

E A Rorke1, G Adhikary2, C A Young2

  • 1Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA.

Cell Death & Disease
|February 20, 2015
PubMed
Summary

Inhibiting Activator Protein 1 (AP1) in mouse epidermis disrupts skin barrier formation, mimicking human keratoderma. This involves altered keratinocyte differentiation, reduced barrier proteins, and changes in gene expression.

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Area of Science:

  • Dermatology
  • Molecular Biology
  • Proteomics

Background:

  • Epidermal keratinocyte differentiation is crucial for skin barrier function.
  • Activator protein 1 (AP1) transcription factors regulate keratinocyte differentiation.
  • AP1 inhibition in mice causes a keratoderma-like phenotype.

Purpose of the Study:

  • To elucidate the structural and molecular changes in TAM67-induced murine keratoderma.
  • To understand the role of AP1 in epidermal differentiation and barrier formation.

Main Methods:

  • Expression of dominant-negative c-jun (TAM67) in murine epidermis.
  • Proteomic analysis of corneocyte cross-linked proteome.
  • RNA array analysis of epidermal gene expression.

Main Results:

  • TAM67-positive epidermis shows altered cornified envelope, reduced barrier integrity, and abnormal keratin and filaggrin processing.
  • Proteomics revealed decreased incorporation of differentiation proteins and increased inflammatory and structural proteins.
  • RNA analysis showed reduced expression of late differentiation genes and increased expression of early differentiation and hyperproliferation genes.

Conclusions:

  • AP1 inactivation in suprabasal epidermis impairs late differentiation gene expression.
  • This leads to compensatory upregulation of early differentiation genes and altered skin barrier structure.
  • Findings provide molecular insights into AP1's role in epidermal homeostasis and disease.