ArticleFrontiers in immunology2019
Role of PKC and ERK Signaling in Epidermal Blistering and Desmosome Regulation in Pemphigus.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 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
- Caspase-activation powers anti-Desmoglein 3-induced acantholysis in human epidermis.Cell death discovery · 2026Article
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- Epac1 contributes to apremilast-mediated rescue of pemphigus autoantibody-induced loss of keratinocyte adhesion.JCI insight · 2025Article
- ERK hyperactivation in epidermal keratinocytes impairs intercellular adhesion and drives Grover disease pathology.JCI insight · 2024Article
- Unbiased screening identifies regulators of cell-cell adhesion and treatment options in pemphigus.Nature communications · 2024Article
- Microarray Gene Expression Analysis of Lesional Skin in Canine Pemphigus Foliaceus.Veterinary sciences · 2024Article
- The impact of signaling pathways on the desmosome ultrastructure in pemphigus.Frontiers in immunology · 2024Article
- Plakophilin 2 regulates intestinal barrier function by modulating protein kinase C activity in vitro.Tissue barriers · 2023Article
- Targeting SERCA2 in organotypic epidermis reveals MEK inhibition as a therapeutic strategy for Darier disease.JCI insight · 2023Article
- Structure and regulation of desmosomes in intercalated discs: Lessons from epithelia.Journal of anatomy · 2023Review
- Mechanisms Causing Acantholysis in Pemphigus-Lessons from Human Skin.Frontiers in immunology · 2022Review
- Dsg1 and Dsg3 Composition of Desmosomes Across Human Epidermis and Alterations in Pemphigus Vulgaris Patient Skin.Frontiers in immunology · 2022Article
- Protein Kinase C-Mediated Hyperphosphorylation and Lateralization of Connexin 43 Are Involved in Autoimmune Myocarditis-Induced Prolongation of QRS Complex.Frontiers in physiology · 2022Article
- Autoantibody-Specific Signalling in Pemphigus.Frontiers in medicine · 2021Review
- Cardiomyocyte adhesion and hyperadhesion differentially require ERK1/2 and plakoglobin.JCI insight · 2020Article
- Dsg2 Upregulation as a Rescue Mechanism in Pemphigus.Frontiers in immunology · 2020Article
- ERK/MEK Pathway Regulates Th17 Cell Differentiation in Patients with Pemphigus Vulgaris.Indian journal of dermatologyArticle
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Desmosomes reinforce cohesion of epithelial cells at the interface between adjacent cells. They include the cadherin-type adhesion molecules desmoglein 1 (Dsg1) and Dsg3. Pemphigus vulgaris (PV) is an autoimmune disease in which circulating autoantibodies (PV-IgG) targeting Dsg1 and 3 cause characteristic epidermal blister formation. It has been shown that PV-IgG binding induced activation of kinases such as ERK and PKC, and inhibition of these signaling pathways prevented loss of cell cohesion in cell cultures. However, the role of Erk and PKC in blister formation and regulation of desmosome ultrastructure in human skin are unknown. Accordingly, we assessed the role of PKC and ERK signaling pathways in blister formation and regulation of desmosome ultrastructure in human epidermis. Here we performed electron microscopy analyses using human skin explants injected with PV-IgG together with inhibitors for PKC or ERK signaling. Inhibition of PKC was not effective to prevent suprabasal blister formation or ultrastructural alterations of desmosomes. In contrast, inhibition of ERK signaling significantly ameliorated blister formation and decrease in the number of desmosomes whereas shortening and splitting of desmosomes and keratin filament insertion were not different from samples treated with PV-IgG alone. However, apical desmosomes between basal and suprabasal cells remained unaltered when ERK signaling was inhibited. Therefore, our results show that inhibition of ERK but not PKC signaling appears to be effective to ameliorate blistering and alterations of desmosome ultrastructure triggered by PV-IgG in human skin.
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