ArticleThe American journal of pathology2011
The extent of desmoglein 3 depletion in pemphigus vulgaris is dependent on Ca(2+)-induced differentiation: a role in suprabasal epidermal skin splitting?
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- What protein kinases are crucial for acantholysis and blister formation in pemphigus vulgaris? A systematic review.Journal of cellular physiology · 2022Pooled it
- Inhibition of the JAK/STAT Signaling Pathway Suggests a Protective Effect against Acantholysis in Pemphigus.Inflammation · 2026Article
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- CaCellular signalling · 2023Review
- Mouse models of pemphigus: valuable tools to investigate pathomechanisms and novel therapeutic interventions.Frontiers in immunology · 2023Review
- Pitfalls in the Application of Dispase-Based Keratinocyte Dissociation Assay for In Vitro Analysis of Pemphigus Vulgaris.Vaccines · 2022Article
- Mechanisms Causing Acantholysis in Pemphigus-Lessons from Human Skin.Frontiers in immunology · 2022Review
- Pemphigus Foliaceus Autoantibodies Induce Redistribution Primarily of Extradesmosomal Desmoglein 1 in the Cell Membrane.Frontiers in immunology · 2022Article
- Modulation of Mechanical Stress Mitigates Anti-Dsg3 Antibody-Induced Dissociation of Cell-Cell Adhesion.Advanced biology · 2021Article
- Autoantibody-Specific Signalling in Pemphigus.Frontiers in medicine · 2021Review
- Dsg2 Upregulation as a Rescue Mechanism in Pemphigus.Frontiers in immunology · 2020Article
- ST18 Enhances PV-IgG-Induced Loss of Keratinocyte Cohesion in Parallel to Increased ERK Activation.Frontiers in immunology · 2019Article
- Role of Dsg1- and Dsg3-Mediated Signaling in Pemphigus Autoantibody-Induced Loss of Keratinocyte Cohesion.Frontiers in immunology · 2019Article
- Role of PKC and ERK Signaling in Epidermal Blistering and Desmosome Regulation in Pemphigus.Frontiers in immunology · 2019Article
- Pemphigus: a Comprehensive Review on Pathogenesis, Clinical Presentation and Novel Therapeutic Approaches.Clinical reviews in allergy & immunology · 2018Review
- Keratin Retraction and Desmoglein3 Internalization Independently Contribute to Autoantibody-Induced Cell Dissociation in Pemphigus Vulgaris.Frontiers in immunology · 2018Article
- Autoantibody Signaling in Pemphigus Vulgaris: Development of an Integrated Model.Frontiers in immunology · 2018Review
- Keratins Regulate p38MAPK-Dependent Desmoglein Binding Properties in Pemphigus.Frontiers in immunology · 2018Article
- Different signaling patterns contribute to loss of keratinocyte cohesion dependent on autoantibody profile in pemphigus.Scientific reports · 2017Article
- Loss of Desmoglein Binding Is Not Sufficient for Keratinocyte Dissociation in Pemphigus.The Journal of investigative dermatology · 2015Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pemphigus vulgaris (PV) is an autoimmune disease of the skin and mucous membranes and is characterized by development of autoantibodies against the desmosomal cadherins desmoglein (Dsg) 3 and Dsg1 and formation of intraepidermal suprabasal blisters. Depletion of Dsg3 is a critical mechanism in PV pathogenesis. Because we did not detect reduced Dsg3 levels in keratinocytes cultured for longer periods under high-Ca(2+) conditions, we hypothesized that Dsg depletion depends on Ca(2+)-mediated keratinocyte differentiation. Our data indicate that depletion of Dsg3 occurs specifically in deep epidermal layers both in skin of patients with PV and in an organotypic raft model of human epidermis incubated using IgG fractions from patients with PV. In addition, Dsg3 depletion and loss of Dsg3 staining were prominent in cultured primary keratinocytes and in HaCaT cells incubated in high-Ca(2+) medium for 3 days, but were less pronounced in HaCaT cultures after 8 days. These effects were dependent on protein kinase C signaling because inhibition of protein kinase C blunted both Dsg3 depletion and loss of intercellular adhesion. Moreover, protein kinase C inhibition blocked suprabasal Dsg3 depletion in cultured human epidermis and blister formation in a neonatal mouse model. Considered together, our data indicate a contribution of Dsg depletion to PV pathogenesis dependent on Ca(2+)-induced differentiation. Furthermore, prominent depletion in basal epidermal layers may contribute to the suprabasal cleavage plane observed in PV.
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