ArticleJCI insight2017
Stat3 regulates desmoglein 3 transcription in epithelial keratinocytes.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Colitis-Associated Colorectal Cancer-STAT3 Inhibition as a Preventive Strategy.International journal of molecular sciences · 2026Article
- Boom or Bust: Clinical Trials in Pemphigus and Other B-Cell-Mediated Autoimmune Diseases.The Journal of investigative dermatology · 2026Review
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- DSG3 promotes bladder cancer growth and metastasis via AKT/GSK3β/β-catenin pathway.Journal of translational medicine · 2025Article
- Mechanisms of Resistance to Rituximab Used for the Treatment of Autoimmune Blistering Diseases.Life (Basel, Switzerland) · 2024Review
- Unbiased screening identifies regulators of cell-cell adhesion and treatment options in pemphigus.Nature communications · 2024Article
- Mouse models of pemphigus: valuable tools to investigate pathomechanisms and novel therapeutic interventions.Frontiers in immunology · 2023Review
- Temporal Outcomes after Rituximab Therapy for Pemphigus Vulgaris.The Journal of investigative dermatology · 2022Article
- Pemphigus and Pemphigoid: From Disease Mechanisms to Druggable Pathways.The Journal of investigative dermatology · 2022Review
- Desmosomal Cadherins in Health and Disease.Annual review of pathology · 2022Review
- Monovalent antibody-conjugated lipid-polymer nanohybrids for active targeting to desmoglein 3 of keratinocytes to attenuate psoriasiform inflammation.Theranostics · 2021Article
- Keratinocyte cadherin desmoglein 1 controls melanocyte behavior through paracrine signaling.Pigment cell & melanoma research · 2020Article
- Tyrosine Kinases in Autoimmune and Inflammatory Skin Diseases.Frontiers in immunology · 2019Review
- Pemphigus: Current and Future Therapeutic Strategies.Frontiers in immunology · 2019Review
- Current Clinical Trials in Pemphigus and Pemphigoid.Frontiers in immunology · 2019Review
- SOX30 is a key regulator of desmosomal gene suppressing tumor growth and metastasis in lung adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2018Article
- Pemphigus-A Disease of Desmosome Dysfunction Caused by Multiple Mechanisms.Frontiers in immunology · 2018Review
- Mechanisms of Autoantibody-Induced Pathology.Frontiers in immunology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pemphigus vulgaris (PV) is an epithelial blistering disease caused by autoantibodies to the desmosomal cadherin desmoglein 3 (DSG3). Glucocorticoids improve disease within days by increasing DSG3 gene transcription, although the mechanism for this observation remains unknown. Here, we show that DSG3 transcription in keratinocytes is regulated by Stat3. Treatment of primary human keratinocytes (PHKs) with hydrocortisone or rapamycin, but not the p38 MAPK inhibitor SB202190, significantly increases DSG3 mRNA and protein expression and correspondingly reduces phospho-S727 Stat3. Stat3 inhibition or shRNA-knockdown also significantly increases DSG3 mRNA and protein levels. Hydrocortisone- or rapamycin-treated PHKs demonstrate increased number and length of desmosomes by electron microscopy and are resistant to PV IgG-induced loss of cell adhesion, whereas constitutive activation of Stat3 in PHKs abrogates DSG3 upregulation and inhibits hydrocortisone and rapamycin's therapeutic effects. Topical hydrocortisone, rapamycin, or Stat3 inhibitor XVIII prevents autoantibody-induced blistering in the PV passive transfer mouse model, correlating with increased epidermal DSG3 expression and decreased phospho-S727 Stat3. Our data indicate that glucocorticoids and rapamycin upregulate DSG3 transcription through inhibition of Stat3. These studies explain how glucocorticoids rapidly improve pemphigus and may also offer novel insights into the physiologic and pathophysiologic regulation of desmosomal cadherin expression in normal epidermis and epithelial carcinomas.
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Registered trials
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.