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Epidermal ADAM17 maintains the skin barrier by regulating EGFR ligand–dependent terminal keratinocyte differentiation
Open accessAbstract
ADAM17 (a disintegrin and metalloproteinase 17) is ubiquitously expressed and cleaves membrane proteins, such as epidermal growth factor receptor (EGFR) ligands, l-selectin, and TNF, from the cell surface, thus regulating responses to tissue injury and inflammation. However, little is currently known about its role in skin homeostasis. We show that mice lacking ADAM17 in keratinocytes (A17ΔKC) have a normal epidermal barrier and skin architecture at birth but develop pronounced defects in epidermal barrier integrity soon after birth and develop chronic dermatitis as adults. The dysregulated expression of epidermal differentiation proteins becomes evident 2 d after birth, followed by reduced transglutaminase (TGM) activity, transepidermal water loss, up-regulation of the proinflammatory cytokine IL-36α, and inflammatory immune cell infiltration. Activation of the EGFR was strongly reduced in A17ΔKC skin, and topical treatment of A17ΔKC mice with recombinant TGF-α significantly improved TGM activity and decreased skin inflammation. Finally, we show that mice lacking the EGFR in keratinocytes (EgfrΔKC) closely resembled A17ΔKC mice. Collectively, these results identify a previously unappreciated critical role of the ADAM17–EGFR signaling axis in maintaining the homeostasis of the postnatal epidermal barrier and suggest that this pathway could represent a good target for treatment of epidermal barrier defects.
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“Epidermal inactivation of EGFR in mice showed that these rashes were a direct consequence of epidermal EGFR, which was attributed to chemokine-driven inflammation51–53.”
From E-cadherin integrates mechanotransduction and EGFR signaling to control junctional tissue polarization and tight junction positioning (2017) · cites this paper as [51]
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Metadata
- Authors
- Franzke, C.-W., Cobzaru, C., Triantafyllopoulou, A., Löffek, S., Horiuchi, K., Threadgill, D. W., Kurz, T., van Rooijen, N., Bruckner-Tuderman, L., & Blobel, C. P.
- Affiliations
- University of Freiburg (DE)
- Keio University (JP)
- North Carolina State University (US)
- Vrije Universiteit Amsterdam (NL)
- Department of Dermatology 1 and 2
- Hospital for Special Surgery (US)
- Corresponding author
- Franzke, Claus-Werner
- Blobel, Carl P.
- ORCID
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2012-05-07
- Volume
- 209
- Issue
- 6
- Pages
- 1105-1119
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC3371728
- OpenAlex
- W2141275577
- Cited by
- 186
- References
- 70
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 11 · 2023: 8 · 2022: 16 · 2021: 11 · 2020: 12 · 2019: 17 · 2018: 12 · 2017: 11 · 2016: 10 · 2015: 16 · 2014: 19 · 2013: 22 · 2012: 2
- FWCI
- 8.94
- Type
- journal article
- Language
- en
- Update notices
- correction (2012-11-26)
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion, other-oa)
- Digital Academic REpository of VU University Amsterdam (Vrije Universiteit Amsterdam) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- European Commission (268390)
- Deutsche Forschungsgemeinschaft (SFB-850/B6, SFB850)
- Albert-Ludwigs-Universität Freiburg
- National Institutes of Health (NIH-R01)
- Medizinische Fakultät der Albert-Ludwigs-Universität Freiburg
- National Cancer Institute (R01CA092479)
- National Institute of General Medical Sciences (R01GM064750, GM-64750)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Skin and Cellular Biology Research
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Dermatology › Genetic and rare skin diseases.
- Keywords
- ADAM17, epidermal growth factor receptor, skin barrier, keratinocyte differentiation, transglutaminase, transepidermal water loss, IL-36α, skin inflammation, chronic dermatitis, transforming growth factor-alpha
- MeSH terms
- ADAM17 Protein, Epidermal Cells, Administration, Topical, Animals, Animals, Newborn, Cell Differentiation, Dermatitis, Atopic, Epidermis, Interleukin-1, Macrophages, Mice, Mutant Strains, Transglutaminases, Skin, Keratinocytes, Transforming Growth Factor alpha, Gene Expression Regulation, Developmental, Mice, ADAM Proteins, ErbB Receptors
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