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Related Concept Videos

Desmosomes01:05

Desmosomes

The term desmosome derives from the Greek words "desmo" and "soma" meaning "adhesion bodies." This structure was first observed during the late 1800s and described as small, dense nodules in the epidermis. Desmosomes are button-like structures that help form an interlinked network of intermediate filaments across the cells. These junctions are  essential to hold cells together under mechanical stress and to maintain tissue integrity. Desmosomes are multi-protein complexes comprising desmosomal...
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Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining. Bicarbonate,...

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Related Experiment Video

Updated: Jul 14, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

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Published on: October 12, 2012

MiR-125b-5p Promotes Pemphigus Vulgaris Pathogenesis by Modulating Desmosome Structures.

Wenxiu He1, Tingning Xiao2, Hong Hua3

  • 1Peking Union Medical College Hospital, Beijing, China.

Bioscience Reports
|July 13, 2026
PubMed
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.

Keywords:
P63PERPdesmosomesmiR-125b-5ppemphigus vulgaris

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Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid
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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.