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The Dishevelled-binding protein CXXC5 negatively regulates cutaneous wound healing

Soung-Hoon Lee1, Mi-Yeon Kim1, Hyun-Yi Kim1

  • 1Translational Research Center for Protein Function Control; Department of Biotechnology, College of Life Science and Biotechnology; and Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, College of Medicine; Yonsei University, Seoul 120-749, South Korea Translational Research Center for Protein Function Control; Department of Biotechnology, College of Life Science and Biotechnology; and Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, College of Medicine; Yonsei University, Seoul 120-749, South Korea.

The Journal of Experimental Medicine
|June 10, 2015
PubMed

Insights

CXXC5 negatively regulates Wnt/β-catenin signaling in skin healing. Inhibiting this interaction accelerates wound repair, suggesting CXXC5 as a therapeutic target for improving cutaneous wound healing.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Regenerative Medicine

Background:

  • Wnt/β-catenin signaling is crucial for skin wound healing and fibrosis.
  • The precise regulatory mechanisms of this pathway remain incompletely understood.
  • A targeted wound-healing agent for this pathway is currently unavailable.

Purpose of the Study:

  • To investigate the role of CXXC-type zinc finger protein 5 (CXXC5) in regulating Wnt/β-catenin signaling during cutaneous wound healing.
  • To explore CXXC5 as a potential therapeutic target for enhancing skin repair.

Main Methods:

  • Investigated CXXC5 protein levels in human wound tissues.
  • Utilized in vitro cell models with CXXC5 overexpression and silencing.
  • Employed CXXC5 knockout mice and a peptide inhibitor (PTD-DBM) of CXXC5-Dvl interaction.
  • Administered PTD-DBM in combination with valproic acid (VPA) in mouse wound models.

Main Results:

  • CXXC5 acts as a negative feedback regulator of Wnt/β-catenin signaling by interacting with Dishevelled (Dvl).
  • CXXC5 protein levels decrease in human wound tissues.
  • CXXC5 deficiency or inhibition accelerates wound healing, enhances collagen production, and promotes myofibroblast differentiation.
  • Combined treatment with PTD-DBM and VPA synergistically improved wound closure in mice.

Conclusions:

  • CXXC5 is a key negative regulator of Wnt/β-catenin signaling in skin.
  • Targeting the CXXC5-Dvl interaction holds promise for developing novel wound-healing therapies.
  • CXXC5 represents a potential therapeutic target for improving cutaneous wound healing and managing dermal fibrosis.

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