Related Experiment Video

Updated: Feb 12, 2026

Isolation, Culture, and Characterization of Primary Schwann Cells, Keratinocytes, and Fibroblasts from Human Foreskin
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Published on: March 23, 2022

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Evidence For a Fibrogenic Interaction Between the Aryl Hydrocarbon Receptor and the Wnt/β-Catenin Pathways in Human

Anna Wajda1, Adam Ejma-Multański1, Dina Himida2

  • 1Department of Molecular Biology, National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|February 11, 2026
PubMed
Abstract

Insights

The aryl hydrocarbon receptor (AHR) plays a key role in skin fibrosis by interacting with TGFβ and Wnt/β-catenin signaling pathways, influencing collagen production and cell migration.

Area of Science:

  • Dermatology
  • Immunology
  • Molecular Biology

Background:

  • Systemic sclerosis is a rare autoimmune fibrotic skin disease.
  • The aryl hydrocarbon receptor (AHR) is crucial for skin homeostasis, but its role in fibrosis is unclear.
  • Investigating the interplay between TGFβ, AHR, and Wnt/β-catenin signaling is important.

Purpose of the Study:

  • To elucidate the role of AHR in skin fibrosis.
  • To understand the crosstalk between TGFβ, AHR, and Wnt/β-catenin signaling in dermal fibroblasts and keratinocytes.

Main Methods:

  • Utilized wild-type and AHR-deficient human dermal fibroblasts and HaCaT keratinocytes.
  • Treated cells with TGFβ and an AHR agonist (FICZ).
  • Assessed collagen type I, MMP1, Wnt/β-catenin gene expression, cell migration, and proteome profiles.

Main Results:

  • AHR deficiency diminished Wnt/β-catenin gene expression and TGFβ-induced collagen production.
  • Co-cultures revealed AHR-dependent regulation of immune-related genes.
  • AHR was essential for scratch closure, indicating a role in cell migration.

Conclusions:

  • AHR exhibits a context-dependent function in skin fibrosis.
  • Demonstrated a significant interaction between AHR, TGFβ, and Wnt/β-catenin signaling in fibrotic processes.
Keywords:
Fibrosis ; Systemic sclerosis ; MMP1 ; Collagen type I ; Aryl hydrocarbon receptor

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