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 skin rashes were a direct consequence of epidermal EGFR, which was attributed to chemokine-driven inflammation.
“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]
The Results section reports that mice with epidermal EGFR inactivation developed inflammatory skin changes, with elevated Ccl2 and Cxcl1 and increased inflammatory-cell infiltrates (page not provided). But the Discussion attributes the inflammation primarily to an earlier skin-barrier defect; it does not establish that chemokines drive the rash. (LLM, conf=0.87)
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- 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)
- Department of Molecular Cell Biology, Faculty of Medicine, Vrije Universiteit, 1081 BT Amsterdam, Netherlands 6
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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