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

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.

You might also read

Related Articles

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

Sort by
Same author

Syntaxin 12 Sustains Endosomal-Lysosomal Homeostasis and Survival in Glioblastoma Stem-Like Cells.

Traffic (Copenhagen, Denmark)·2026
Same author

From tumor-centric to ecosystem-based hypotheses in brain tumor research and care: Proceedings from The second Brain Tumor Meeting by the Sea organized by Julie Gavard and Eric Chevet, held in St Malo (France), 23-25 March 2026.

Molecular oncology·2026
Same author

Linear ubiquitin chain assembly complex contributes to NLRP3-mediated pyroptotic cell death.

iScience·2026
Same author

Traffic Light Commentary-Src in the Upside Down: A Kinase Turned Inside Out.

Traffic (Copenhagen, Denmark)·2026
Same author

When the Lights Go Out: The Challenge of Neuroabandonment.

AJOB neuroscience·2026
Same author

A unique malignant cell type per patient tumor encoded in each cancer cell transcriptome.

iScience·2026

Related Experiment Video

Updated: May 21, 2026

Evaluating Vascular Hyperpermeability-inducing Agents in the Skin with the Miles Assay
08:43

Evaluating Vascular Hyperpermeability-inducing Agents in the Skin with the Miles Assay

Published on: June 19, 2018

Semaphorin 3A elevates endothelial cell permeability through PP2A inactivation.

Armelle Le Guelte1, Eva-Maria Galan-Moya, Julie Dwyer

  • 1Cnrs, UMR8104, 75014 Paris, France.

Journal of Cell Science
|June 12, 2012
PubMed
Summary

Semaphorin 3A triggers vascular leakage by destabilizing cell junctions in brain endothelial cells. This occurs via disrupting the PP2A phosphatase and VE-cadherin interaction, increasing brain endothelial permeability.

More Related Videos

An in vivo Assay to Test Blood Vessel Permeability
07:03

An in vivo Assay to Test Blood Vessel Permeability

Published on: March 16, 2013

Human Saphenous Vein Endothelial Cell Isolation and Exposure to Controlled Levels of Shear Stress and Stretch
09:10

Human Saphenous Vein Endothelial Cell Isolation and Exposure to Controlled Levels of Shear Stress and Stretch

Published on: April 21, 2023

Related Experiment Videos

Last Updated: May 21, 2026

Evaluating Vascular Hyperpermeability-inducing Agents in the Skin with the Miles Assay
08:43

Evaluating Vascular Hyperpermeability-inducing Agents in the Skin with the Miles Assay

Published on: June 19, 2018

An in vivo Assay to Test Blood Vessel Permeability
07:03

An in vivo Assay to Test Blood Vessel Permeability

Published on: March 16, 2013

Human Saphenous Vein Endothelial Cell Isolation and Exposure to Controlled Levels of Shear Stress and Stretch
09:10

Human Saphenous Vein Endothelial Cell Isolation and Exposure to Controlled Levels of Shear Stress and Stretch

Published on: April 21, 2023

Area of Science:

  • Neuroscience
  • Cell Biology
  • Oncology

Background:

  • Vascular endothelial cadherin (VE-cadherin) mediates cell-cell junctions, controlling paracellular permeability.
  • Angiogenic and inflammatory stimuli weaken VE-cadherin, increasing vascular permeability.
  • Semaphorin 3A is an anti-angiogenic factor with known pro-permeability effects, but its mechanism is unclear.

Purpose of the Study:

  • To elucidate the mechanism by which Semaphorin 3A induces vascular leakage in brain endothelial cells.
  • To investigate the role of Semaphorin 3A secreted by glioma cells in promoting brain endothelial permeability.

Main Methods:

  • Investigated Semaphorin 3A effects on VE-cadherin phosphorylation and internalization in brain endothelial cells.
  • Assessed the impact of Semaphorin 3A on cell-cell junction stability and barrier integrity.
  • Examined the interaction between Semaphorin 3A, protein phosphatase 2A (PP2A), and VE-cadherin.
  • Utilized pharmacological inhibition and siRNA knockdown of PP2A to study its role.

Main Results:

  • Semaphorin 3A induced VE-cadherin serine phosphorylation and internalization, destabilizing cell junctions and reducing barrier integrity.
  • Tumor-initiating cells from high-grade gliomas secreted Semaphorin 3A, increasing brain endothelial monolayer permeability.
  • Semaphorin 3A inhibited PP2A activity and disrupted its interaction with VE-cadherin.
  • PP2A inhibition or knockdown mimicked Semaphorin 3A's effects on VE-cadherin and permeability.

Conclusions:

  • Semaphorin 3A contributes to elevated vascular permeability by disrupting the PP2A/VE-cadherin balance in brain endothelial cells.
  • Local Semaphorin 3A production, particularly from gliomas, can enhance brain endothelial permeability.
  • Targeting the PP2A/VE-cadherin pathway may offer therapeutic strategies for conditions involving increased vascular permeability.