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

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

511
Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
511
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

2.7K
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
2.7K
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

826
Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
826
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

4.9K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
4.9K
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

1.6K
Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
1.6K
Bioactivation and Tissue Toxicity01:25

Bioactivation and Tissue Toxicity

69
Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...
69

You might also read

Related Articles

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

Sort by
Same author

A miR-382-5p-PORCN axis modulates endogenous Wnt signaling during palatal development.

Biochemical and biophysical research communications·2026
Same author

Green synthesized Cu<sub>2</sub>O/TiO<sub>2</sub> nanotube heterojunction for pharmaceutical mineralization and simultaneous hydrogen evolution: mechanistic insight and toxicity assessment.

Journal of environmental management·2026
Same author

Real-world emission factors and inhalation health risks of PM-bound metals from workboats using ultra-low sulfur marine fuel.

Environmental pollution (Barking, Essex : 1987)·2026
Same author

Cocktail-like alginate-derived carbonized nanogels with diverse moieties attenuate tumor metastasis via potential multi-pathway modulation.

International journal of biological macromolecules·2026
Same author

Carbonization of citrus-derived flavonoids exhibits enhanced anti-coronavirus infection in vitro and in vivo.

International journal of biological macromolecules·2026
Same author

High-throughput generation of patient-derived cancer stem cells for precision medicine using a microwell-chip platform.

Nature cell biology·2026

Related Experiment Video

Updated: Mar 2, 2026

Using En Face Immunofluorescence Staining to Observe Vascular Endothelial Cells Directly
06:09

Using En Face Immunofluorescence Staining to Observe Vascular Endothelial Cells Directly

Published on: August 20, 2019

17.1K

Carbon black aggregates cause endothelial dysfunction by activating ROCK.

Junyan Yan1, Chia-Hsiang Lai2, Shih-Chun Candice Lung3

  • 1Key Laboratory of Nano-Bio Interface, Division of Nanobiomedicine, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Suzhou 215123, China; University of Chinese Academy of Sciences, Beijing 100039, China.

Journal of Hazardous Materials
|May 23, 2017
PubMed
Summary
This summary is machine-generated.

Aggregated carbon black nanoparticles (CBAs) harm vascular cells by activating Rho-associated kinase (ROCK). Inhibiting ROCK reduces CBA-induced endothelial dysfunction, cytoskeletal damage, and inflammation, suggesting ROCK as a therapeutic target.

Keywords:
AggregateCarbon blackEndothelial dysfunctionRho-associated kinase

More Related Videos

Assessment of Vascular Function in Patients With Chronic Kidney Disease
08:50

Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

16.9K
Visualization of Vascular Ca2+ Signaling Triggered by Paracrine Derived ROS
07:33

Visualization of Vascular Ca2+ Signaling Triggered by Paracrine Derived ROS

Published on: December 21, 2011

16.1K

Related Experiment Videos

Last Updated: Mar 2, 2026

Using En Face Immunofluorescence Staining to Observe Vascular Endothelial Cells Directly
06:09

Using En Face Immunofluorescence Staining to Observe Vascular Endothelial Cells Directly

Published on: August 20, 2019

17.1K
Assessment of Vascular Function in Patients With Chronic Kidney Disease
08:50

Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

16.9K
Visualization of Vascular Ca2+ Signaling Triggered by Paracrine Derived ROS
07:33

Visualization of Vascular Ca2+ Signaling Triggered by Paracrine Derived ROS

Published on: December 21, 2011

16.1K

Area of Science:

  • Toxicology
  • Nanotechnology
  • Cardiovascular Biology

Background:

  • Carbon black nanoparticles (CBNs) are linked to atherosclerosis progression.
  • Previous studies focused on nano-sized particles, not aggregates, in endothelial dysfunction.
  • Endothelial cells form the inner lining of blood vessels and are crucial for vascular health.

Purpose of the Study:

  • To investigate the endothelial toxicity of carbon black aggregates (CBAs) in human EA.hy926 vascular cells.
  • To determine the role of Rho-associated kinase (ROCK) in CBA-induced endothelial dysfunction.

Main Methods:

  • Exposure of EA.hy926 cells to varying concentrations of CBAs.
  • Assessment of cell viability, lactate dehydrogenase leakage, and oxidative stress.
  • Transmission electron microscopy (TEM) to visualize CBA uptake.
  • Co-treatment with a ROCK inhibitor (Y-27632) to evaluate ROCK pathway involvement.

Main Results:

  • High concentrations of CBAs reduced cell viability, increased LDH leakage, and induced oxidative stress.
  • TEM revealed CBA entry into cells via membrane-enclosed vesicles.
  • Co-treatment with Y-27632 significantly attenuated CBA-induced cytoskeletal damage, endothelial barrier dysfunction, and inflammatory factor expression.

Conclusions:

  • Aggregated carbon black nanoparticles induce endothelial dysfunction.
  • This dysfunction may occur through the activation of the Rho-associated kinase (ROCK) pathway.
  • ROCK inhibition shows potential in mitigating the adverse effects of CBAs on vascular cells.