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 Experiment Videos

TNF-alpha induces endothelial cell F-actin depolymerization, new actin synthesis, and barrier dysfunction

S E Goldblum1, X Ding, J Campbell-Washington

  • 1Department of Medicine, Department of Veterans Affairs Medical Center, Baltimore, Maryland.

The American Journal of Physiology
|April 1, 1993
PubMed
Summary

Tumor necrosis factor-alpha (TNF-alpha) disrupts pulmonary vascular endothelial barrier function by causing actin reorganization. This leads to increased permeability and cell gaps, suggesting a novel therapeutic target.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Random regression modelling of genetic covariance when data are available for litters: an application in mice.

Animal : an international journal of animal bioscience·2026
Same author

[Clinical characteristics of diarrhea caused by rotavirus A in children under 5 years old in China, 2009-2020].

Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi·2026
Same author

[Prevalence, treatment, and control trends of cardiovascular risk factors among the young adults in the Kailuan study from 2006 to 2020].

Zhonghua xin xue guan bing za zhi·2026
Same author

The alleviating effect of dietary electrolyte balance levels on heat stress <i>via</i> regulating water and ion metabolism in Pekin ducks.

British poultry science·2026
Same author

Integrating eQTL and genome-wide association studies to uncover additive and dominant regulatory circuits in pig uterine capacity.

Animal : an international journal of animal bioscience·2025
Same author

[Retrospective analysis of the etiology and treatment of 20 cases of retrograde peri-implantitis].

Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology·2025

Area of Science:

  • Pulmonary vascular biology
  • Cellular signaling
  • Inflammation research

Background:

  • Tumor necrosis factor-alpha (TNF-alpha) is a key inflammatory cytokine.
  • Endothelial barrier function is critical for regulating vascular permeability.
  • The role of TNF-alpha in pulmonary endothelial barrier integrity is not fully understood.

Purpose of the Study:

  • To investigate whether recombinant TNF-alpha (rTNF-alpha) regulates pulmonary vascular endothelial barrier function via actin reorganization.
  • To elucidate the mechanisms by which rTNF-alpha affects endothelial cell actin cytoskeleton and barrier integrity.

Main Methods:

  • Bovine pulmonary artery endothelial cell monolayers were treated with rTNF-alpha.
  • Assays included transendothelial albumin flux, F-actin and G-actin levels, and intercellular gap formation.

Related Experiment Videos

  • Fluorescence microscopy and spectrofluorometry were used to assess actin organization and quantity.

    • Main Results:

    • rTNF-alpha increased albumin flux and intercellular gap formation, indicating barrier dysfunction.
    • rTNF-alpha induced a decrease in F-actin and a reciprocal increase in G-actin.
    • Stabilizing F-actin protected against rTNF-alpha-induced barrier changes, while inhibiting protein synthesis exacerbated them.

    Conclusions:

    • rTNF-alpha directly causes pulmonary vascular endothelial F-actin depolymerization, leading to intercellular gap formation and barrier dysfunction.
    • Increased actin synthesis may represent a compensatory response to rTNF-alpha-induced F-actin loss.
    • Targeting TNF-alpha-mediated actin dynamics could offer therapeutic strategies for pulmonary vascular diseases.