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Updated: Jun 11, 2025

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Generation and Culturing of Primary Human Keratinocytes from Adult Skin
Published on: December 22, 2017
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Inflammatory Mediators Suppress FGFR2 Expression in Human Keratinocytes to Promote Inflammation
Luca Ferrarese1, Michael Koch1, Artemis Baumann1
1Institute of Molecular Health Sciences, Department of Biology, ETH Zürich, Zürich, Switzerland.
Molecular and Cellular Biology
|September 28, 2024
Summary
Fibroblast Growth Factor Receptor 2 (FGFR2) deficiency in human skin cells promotes inflammation. Reduced FGFR2 in atopic dermatitis patients may worsen skin inflammation.
Area of Science:
- Dermatology
- Molecular Biology
- Immunology
Background:
- Fibroblast growth factors (FGFs) and their receptors (FGFRs) are crucial for tissue regulation.
- FGFR deficiency in mouse skin cells causes inflammation resembling atopic dermatitis, but human relevance is unknown.
Purpose of the Study:
- To investigate the role of Fibroblast Growth Factor Receptor 2 (FGFR2) in human keratinocytes.
- To determine the relevance of FGFR2 in atopic dermatitis pathogenesis.
Main Methods:
- Generated human keratinocytes with CRISPR/Cas9-induced FGFR2 knockout.
- Analyzed gene expression changes under homeostatic and inflammatory conditions.
- Performed bioinformatics analysis of RNA-seq data from patient skin samples.
Main Results:
- FGFR2 knockout keratinocytes showed increased expression of interferon-stimulated genes and pro-inflammatory cytokines.
- FGFR2 expression decreased in human keratinocytes upon exposure to inflammatory stimuli.
- Reduced FGFR2 expression was observed in lesional skin of atopic dermatitis patients.
Conclusions:
- FGFR2 plays a critical role in suppressing inflammation in human keratinocytes.
- Downregulation of FGFR2 may contribute to atopic dermatitis and other inflammatory skin conditions.
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