ArticleThe American journal of pathology2009
Keratinocyte but not endothelial cell-specific overexpression of Tie2 leads to the development of psoriasis.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 85 citations in OpenAlex.
- Oxymatrine therapy inhibited epidermal cell proliferation and apoptosis in severe plaque psoriasis.The British journal of dermatology · 2019Trial
- Restoration of Keratinocyte Homeostasis Drives Resolution of Skin Inflammation.bioRxiv : the preprint server for biology · 2026Article
- G-CSF Mediates Increased Renal Neutrophils and Kidney Damage in a Psoriasis Mouse Model.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Neuroimmunology of psoriasis: Possible roles for calcitonin gene-related peptide in its pathogenesis.Brain, behavior, & immunity - health · 2025Review
- Macrophage Functions in Psoriasis: Lessons from Mouse Models.International journal of molecular sciences · 2024Review
- Suppression of TCF4 promotes a ZC3H12A-mediated self-sustaining inflammatory feedback cycle involving IL-17RA/IL-17RE epidermal signaling.JCI insight · 2024Article
- RNA-Based Antipsoriatic Gene Therapy: An Updated Review Focusing on Evidence from Animal Models.Drug design, development and therapy · 2024Review
- Evaluation ofMediators of inflammation · 2024Article
- Control of myeloid cell functions by nociceptors.Frontiers in immunology · 2023Review
- Mouse Models of Psoriasis: A Comprehensive Review.The Journal of investigative dermatology · 2022Review
- Updated Perspectives on Keratinocytes and Psoriasis: Keratinocytes are More Than Innocent Bystanders.Psoriasis (Auckland, N.Z.) · 2022Review
- IFN-κ Is a Rheostat for Development of Psoriasiform Inflammation.The Journal of investigative dermatology · 2022Article
- Roles of calcitonin gene-related peptide in the skin, and other physiological and pathophysiological functions.Brain, behavior, & immunity - health · 2021Review
- New Frontiers in Psoriatic Disease Research, Part I: Genetics, Environmental Triggers, Immunology, Pathophysiology, and Precision Medicine.The Journal of investigative dermatology · 2021Review
- Methods to label, image, and analyze the complex structural architectures of microvascular networks.Microcirculation (New York, N.Y. : 1994) · 2019Review
- Type1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis.Frontiers in immunology · 2019Review
- Epithelial TRAF6 drives IL-17-mediated psoriatic inflammation.JCI insight · 2018Article
- Protection from Psoriasis-Related Thrombosis after Inhibition of IL-23 or IL-17A.The Journal of investigative dermatology · 2018Article
- Research Techniques Made Simple: Murine Models of Human Psoriasis.The Journal of investigative dermatology · 2018Review
- Models in the Research Process of Psoriasis.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Psoriasis is initiated and maintained through a multifaceted interplay between keratinocytes, blood vessels, gene expression, and the immune system. One previous psoriasis model demonstrated that overexpression of the angiopoietin receptor Tie2 in endothelial cells and keratinocytes led to the development of a psoriasiform phenotype; however, the etiological significance of overexpression in each cell type alone was unclear. We have now engineered two new mouse models whereby Tie2 expression is confined to either endothelial cells or keratinocytes. Both lines of mice have significant increases in dermal vasculature but only the KC-Tie2-overexpressing mice developed a cutaneous psoriasiform phenotype. These mice spontaneously developed characteristic hallmarks of human psoriasis, including extensive acanthosis, increases in dermal CD4(+) T cells, infiltrating epidermal CD8(+) T cells, dermal dendritic cells and macrophages, and increased expression of cytokines and chemokines associated with psoriasis, including interferon-gamma, tumor necrosis factor-alpha, and interleukins 1alpha, 6, 12, 22, 23, and 17. Host-defense molecules, cathelicidin, beta-defensin, and S100A8/A9, were also up-regulated in the hyperproliferative skin. All of the phenotypic traits were completely reversed without any scarring following repression of the transgene and were significantly improved following treatment with the anti-psoriasis systemic therapeutic, cyclosporin A. Therefore, confining Tie2 overexpression solely to keratinocytes results in a mouse model that meets the clinical, histological, immunophenotypic, biochemical, and pharmacological criteria required for an animal model of human psoriasis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.