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Selective Inhibition of β-Catenin/Co-Activator Cyclic AMP Response Element-Binding Protein-Dependent Signaling

Haruna Matsuda-Hirose1, Tomoko Yamate1, Mizuki Goto1

  • 1Department of Dermatology, Faculty of Medicine, Oita University, Oita, Japan.

Annals of Dermatology
|April 29, 2021
PubMed
Abstract

Insights

ICG-001, a Wnt/β-catenin signaling inhibitor, effectively normalized skin barrier function and inflammation in an atopic dermatitis (AD) mouse model. This suggests targeting β-catenin/cyclic AMP response element-binding protein (CBP) signaling is a promising therapeutic strategy for AD.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Immunology

Background:

  • The Wnt/β-catenin signaling pathway regulates critical biological processes.
  • ICG-001 inhibits the β-catenin/cyclic AMP response element-binding protein (CBP) interaction.
  • ICG-001 has shown efficacy in various Wnt-driven disease models, but its role in atopic dermatitis (AD) is unexplored.

Purpose of the Study:

  • To determine if β-catenin/CBP signaling contributes to AD pathogenesis.
  • To evaluate ICG-001 as a potential therapeutic agent for AD.

Main Methods:

  • An AD-like murine model was established using topical oxazolone (Ox) application.
  • Mice received daily intraperitoneal injections of ICG-001 or vehicle during dermatitis development.

Main Results:

  • ICG-001 treatment normalized key AD markers, including transepidermal water loss, epidermal and dermal thickness, and stratum corneum hydration.
  • Oxazolone-induced increases in myofibroblast and mast cell counts, and serum levels of thymic stromal lymphopoietin and thymus and activation-regulated chemokine were reversed by ICG-001.
  • Elevated serum periostin levels showed a non-significant trend toward downregulation with ICG-001 treatment.

Conclusions:

  • β-catenin/CBP-dependent signaling appears to play a role in AD pathogenesis.
  • ICG-001 demonstrates therapeutic potential for treating atopic dermatitis.
Keywords:
Atopic dermatitisMouseTherapy

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