ArticleCell death & disease2024
GRHL2 regulates keratinocyte EMT-MET dynamics and scar formation during cutaneous wound healing.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- ML281 Does Not Function as an STK33 Inhibitor but Modulates Proliferation and Differentiation of Keratinocytes Derived from Hypertrophic Scars.International journal of molecular sciences · 2026Article
- Fluctuating environment causes neoplastic transition and epithelial-mesenchymal plasticity in human cells.Research square · 2026Article
- H3K9me3 controls epidermis morphogenesis by regulating RNA Pol II dynamics at developmental promoters and enhancers.Nature communications · 2026Article
- Tick Extracellular Vesicles Alter Epidermal Keratinocyte Function.The Journal of investigative dermatology · 2026Article
- 3D organotypic skin models recapitulate autoantibody-driven pemphigus pathomechanisms and targeted therapeutic response.Science advances · 2026Article
- Single-Cell RNA-Seq Reveals a Glycolysis-Biased EMT State in Keloid Keratinocytes That Amplifies the Pro-Inflammatory and Fibrotic Microenvironment.Journal of inflammation research · 2026Article
- Machine learning multiomics Deciphers GRHL2 associated tumor microenvironment evolution guiding precision therapeutics in breast cancer.Discover oncology · 2025Article
- Gene Therapies in Dermatological Diseases: A Breakthrough in Treatment.International journal of molecular sciences · 2025Review
- Transition paths across the epithelial-mesenchymal transition landscape are dictated by network logic.Development (Cambridge, England) · 2025Article
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Authors and funding
5 authors.
Funding
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Abstract
After cutaneous wounds successfully heal, keratinocytes that underwent the epithelial-mesenchymal transition (EMT) regain their epithelial characteristics, while in scar tissue, epidermal cells persist in a mesenchymal state. However, the regulatory mechanisms governing this reversion are poorly understood, and the impact of persistent mesenchymal-like epidermal cells in scar tissue remains unclear. In the present study, we found that during wound healing, the regulatory factor GRHL2 is highly expressed in normal epidermal cells, downregulated in EMT epidermal cells, and upregulated again during the process of mesenchymal-epithelial transition (MET). We further demonstrated that interfering with GRHL2 expression in epidermal cells can effectively induce the EMT. Conversely, the overexpression of GRHL2 in EMT epidermal cells resulted in partial reversion of the EMT to an epithelial state. To investigate the effects of failed MET in epidermal cells on skin wound healing, we interfered with GRHL2 expression in epidermal cells surrounding the cutaneous wound. The results demonstrated that the persistence of epidermal cells in the mesenchymal state promoted fibrosis in scar tissue, manifested by increased thickness of scar tissue, deposition of collagen and fibronectin, as well as the activation of myofibroblasts. Furthermore, the miR-200s/Zeb1 axis was perturbed in GRHL2 knockdown keratinocytes, and transfection with miR-200s analogs promoted the reversion of EMT in epidermal cells, which indicates that they mediate the EMT process in keratinocytes. These results suggest that restoration of the epithelial state in epidermal cells following the EMT is essential to wound healing, providing potential therapeutic targets for preventing scar formation.
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