Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Skin Diseases and Disorders01:23

Skin Diseases and Disorders

4.1K
Skin is the first line of defense and encounters a variety of microbes. Some pathogenic strains are often the cause of a broad range of infections of the skin and other body systems. These conditions can affect people of all ages and may have different causes, including genetic factors, infections, autoimmune reactions, environmental factors, and lifestyle choices.
Gram-positive Staphylococcus spp. and Streptococcus spp. are responsible for many of the most common skin infections. However, many...
4.1K
Desmosomes01:05

Desmosomes

5.6K
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...
5.6K
Pigmentation01:19

Pigmentation

2.6K
The color of the skin is influenced by a number of pigments, including melanin, carotene, and hemoglobin. Recall that melanin is produced by cells called melanocytes, which are found scattered throughout the stratum basale of the epidermis. The melanin is transferred to the keratinocytes via melanosomes.
Melanin occurs in two primary forms: eumelanin that provides black and brown pigment and pheomelanin that provides red color. Dark-skinned individuals produce more melanin than those with pale...
2.6K
Renewal of Skin Epidermal Stem Cells01:12

Renewal of Skin Epidermal Stem Cells

2.6K
The skin is divided into epidermis, dermis, and hypodermis, the skin's outermost, middle, and inner layers. The human epidermal layer regularly undergoes renewal, where old, dead cells are replaced by new cells. Epidermal stem cells or EpiSCs divide and differentiate to restore the lost cells. For the renewal process, some EpiSCs continuously self-renew. In contrast, few others differentiate into transit-amplifying cells, which later form prickle or spinous cells, followed by granular...
2.6K
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

811
Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
811
Cytoskeletal Linker Proteins - Plakins01:09

Cytoskeletal Linker Proteins - Plakins

2.4K
Plakins are large proteins with binding domains for microtubules, microfilaments, intermediate filaments, and membrane-associated protein complexes at cell junctions. Plakin functions are evolutionarily conserved and are primarily involved in organizing the different components of the cytoskeleton by crosslinking them to each other and connecting them to the cell-matrix and cell adhesion complexes. They are also known to interact with signal transducers, serve as scaffolds for signaling...
2.4K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Erlotinib impairs epidermal tight junction and barrier integrity by inhibiting EGFR and Src and affects maturation of cell-cell junctions in human and mouse keratinocytes.

Tissue barriers·2026
Same author

A Dsg3-specific pemphigus autoantibody induces formation of immature desmosomes associated with impaired adhesion.

Tissue barriers·2026
Same author

Autoantibodies in Patients With Arrhythmogenic Cardiomyopathy Activate GSK-3β, Resulting in a Loss of Cardiomyocyte Cohesion.

Acta physiologica (Oxford, England)·2026
Same author

Cuticular Hydrocarbon Composition of Adhesive Secretions from Functionally Different Attachment Pads of the Stick Insect Medauroidea extradentata (Phasmatodea).

Journal of chemical ecology·2026
Same author

Butterfly Diversity in a Sacred Kaya Forest in Southern Kenya.

Ecology and evolution·2026
Same author

STED/AFM as a tool to investigate mechanical and adhesive properties of migrating keratinocytes.

Cell adhesion & migration·2026

Related Experiment Video

Updated: Sep 7, 2025

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

10.6K

Mechanisms Causing Acantholysis in Pemphigus-Lessons from Human Skin.

Desalegn Tadesse Egu1, Thomas Schmitt1, Jens Waschke1

  • 1Chair of Vegetative Anatomy, Institute of Anatomy, Faculty of Medicine, Ludwig-Maximilians-Universität Munich, Munich, Germany.

Frontiers in Immunology
|June 20, 2022
PubMed
Summary

Pemphigus vulgaris (PV) blistering is reduced by inhibiting specific signaling pathways like ERK and PLC/Ca2+ in human skin. These pathways are crucial for maintaining desmosome structure and keratin filament attachment, offering new therapeutic targets for PV.

Keywords:
desmosomeselectron microscopeex vivo skin modelpemphigussignalingultrastructure

More Related Videos

A Simplified and Efficient Method to Isolate Primary Human Keratinocytes from Adult Skin Tissue
06:17

A Simplified and Efficient Method to Isolate Primary Human Keratinocytes from Adult Skin Tissue

Published on: August 25, 2018

10.3K
Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin
10:51

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin

Published on: July 14, 2017

31.5K

Related Experiment Videos

Last Updated: Sep 7, 2025

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

10.6K
A Simplified and Efficient Method to Isolate Primary Human Keratinocytes from Adult Skin Tissue
06:17

A Simplified and Efficient Method to Isolate Primary Human Keratinocytes from Adult Skin Tissue

Published on: August 25, 2018

10.3K
Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin
10:51

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin

Published on: July 14, 2017

31.5K

Area of Science:

  • Dermatology
  • Cell Biology
  • Immunology

Background:

  • Pemphigus vulgaris (PV) is an autoimmune blistering disease targeting desmosomal proteins desmoglein 1 and 3.
  • PV pathogenesis involves autoantibodies (PV-IgG) disrupting desmosome structure and keratin filament adhesion.
  • Intracellular signaling pathways downstream of PV-IgG binding contribute to PV pathology.

Purpose of the Study:

  • To investigate the role of signaling pathways in PV pathogenesis using an ex vivo human skin model.
  • To characterize the ultrastructural effects of PV-IgG on desmosomes and identify protective signaling targets.
  • To evaluate the efficacy of inhibiting specific signaling pathways in preventing PV-induced skin blistering.

Main Methods:

  • Utilized transmission electron microscopy to analyze desmosome ultrastructure in an ex vivo human skin model.
  • Assessed blister formation and scores following inhibition of various signaling pathways (p38MAPK, ERK, PLC/Ca2+, Src, PKC).
  • Correlated ultrastructural changes with the effects of signaling pathway inhibition on desmosome integrity and keratin filament attachment.

Main Results:

  • Inhibition of p38MAPK, ERK, and PLC/Ca2+ pathways demonstrated a protective effect against blistering in human skin explants.
  • Inhibition of Src and PKC pathways was not protective in the human skin model, unlike in cell cultures or murine models.
  • Maintaining desmosome number (via ERK) and keratin filament insertion (via PLC/Ca2+) are critical for preventing skin blistering.

Conclusions:

  • Signaling pathways like ERK and PLC/Ca2+ are key targets for preventing pemphigus vulgaris skin blistering.
  • p38MAPK regulates multiple aspects of desmosome turnover, including number, size, and keratin insertion.
  • Ultrastructural analysis in human skin models provides specific insights into the roles of signaling molecules in desmosome dynamics and potential therapeutic strategies for PV.