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Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin
10:51

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin

Published on: July 14, 2017

Fibroblast growth factor receptors 1 and 2 in keratinocytes control the epidermal barrier and cutaneous homeostasis

Jingxuan Yang1, Michael Meyer, Anna-Katharina Müller

  • 1Department of Biology, Institute of Cell Biology, Eidgenössische Technische Hochschule Zurich, 8093 Zurich, Switzerland.

The Journal of Cell Biology
|March 24, 2010
PubMed

Insights

Fibroblast growth factors (FGFs) are crucial for skin health. Loss of FGF receptor signaling in skin cells leads to barrier defects, inflammation, and loss of skin appendages.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Immunology

Background:

  • Fibroblast growth factors (FGFs) are key regulators of organogenesis and tissue homeostasis.
  • FGF signaling pathways, mediated by FGF receptors (FGFRs), play vital roles in skin development and maintenance.

Purpose of the Study:

  • To investigate the specific functions of FGFRs in skin homeostasis and disease.
  • To elucidate the mechanisms by which FGFR signaling regulates epidermal barrier function and prevents inflammation.

Main Methods:

  • Utilized genetically engineered mice with deficiencies in specific FGFR splice variants (IIIb) in keratinocytes.
  • Analyzed skin phenotypes, including appendage development, inflammation, and epidermal structure.
  • Investigated molecular mechanisms involving tight junctions, cytokine production, and cell signaling.

Main Results:

  • Loss of FGFR1 and FGFR2 IIIb variants in keratinocytes resulted in progressive loss of skin appendages, inflammation, hyperproliferation, and acanthosis.
  • Defective FGF signaling led to reduced expression of tight junction proteins, compromising epidermal barrier function.
  • The compromised barrier triggered keratinocyte and gammadelta T cell activation, producing inflammatory cytokines (IL-1 family member 8, S100A8/A9).
  • A paracrine loop involving dermal cells producing keratinocyte mitogens exacerbated the inflammatory response.

Conclusions:

  • FGF signaling is essential for maintaining epidermal barrier integrity and preventing cutaneous inflammation.
  • Disruptions in FGF-FGFR signaling in skin can lead to inflammatory skin diseases.
  • Stromal-epithelial interactions are critical for skin homeostasis and are significantly influenced by FGF signaling.

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