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Granulocyte-dependent Autoantibody-induced Skin Blistering
Published on: October 12, 2012
MiR-125b-5p promotes pemphigus vulgaris pathogenesis by modulating desmosome structures
Wenxiu He1,2,3, Tingning Xiao2, Hong Hua2
1Department of Stomatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, PR China.
Bioscience Reports
|July 13, 2026
Summary
MicroRNA-125b-5p exacerbates pemphigus vulgaris by targeting P63, reducing P63 and PERP expression. This leads to damaged desmosomes and impaired skin barrier function in this autoimmune disease.
Area of Science:
- Dermatology
- Molecular Biology
- Immunology
Background:
- Pemphigus vulgaris (PV) is a severe autoimmune blistering disease with unknown pathogenesis.
- Previous studies show elevated miR-125b-5p in PV patients.
- miR-125b-5p targets P63 mRNA, inhibiting P63 expression, which regulates PERP.
Purpose of the Study:
- To investigate the role of miR-125b-5p, P63, and PERP in PV pathogenesis.
- To explore the molecular mechanisms by which miR-125b-5p affects desmosome integrity.
Main Methods:
- Dual-luciferase reporter assay to confirm miR-125b-5p binding to P63 3' UTR.
- In vitro culture of mouse tongue tissues treated with anti-Dsg3 mAb and/or miR-125b-5p.
- Analysis of P63 and PERP mRNA/protein levels.
- Transmission electron microscopy (TEM) to assess desmosome structure.
Main Results:
- miR-125b-5p directly inhibits P63 expression.
- Overexpression of miR-125b-5p reduced P63 and PERP levels in Dsg3-mAb-treated tissues.
- TEM revealed increased interdesmosal width, reduced keratin insertion, and damaged desmosomes with miR-125b-5p overexpression.
Conclusions:
- miR-125b-5p contributes to PV pathogenesis by targeting P63.
- This mechanism disrupts desmosome integrity through reduced P63 and PERP expression.
- miR-125b-5p represents a potential therapeutic target for pemphigus vulgaris.
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