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

Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

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...
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

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 (ECE). Of...
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

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...
Cholesterol: Significance and Regulation01:29

Cholesterol: Significance and Regulation

Although not a source of energy, cholesterol plays a significant role as a foundational structure for bile salts, steroid hormones, and vitamin D, as well as being a crucial component of plasma membranes. Approximately 15% of blood cholesterol is derived from our diet, with the remainder synthesized from acetyl CoA by the liver and intestines. Cholesterol is eliminated from the body through its conversion into bile salts, which are eventually discarded in the feces.
Considering cholesterol and...

You might also read

Related Articles

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

Sort by
Same author

Smokeless tobacco consumption induces dysbiosis of oral mycobiome: a pilot study.

Applied microbiology and biotechnology·2022
Same author

Hsp90 and Associated Co-Chaperones of the Malaria Parasite.

Biomolecules·2022
Same author

A rare case of secondary haemophagocytic lymphohistiocytosis in visceral leishmaniasis.

Tropical doctor·2022
Same author

An 80-year-old woman with myelofibrosis and diffuse mosaic attenuation on chest computed tomography.

Respiratory medicine case reports·2022
Same author

Applicability of Adults 2015 American Thyroid Association Differentiated Thyroid Cancer Guidelines for Postoperative Risk Stratification and Postradioiodine Treatment Dynamic Risk Stratification in Pediatric Population.

World journal of nuclear medicine·2022
Same author

Development of the India COVID-19 vaccine tracker.

The Indian journal of medical research·2022

Related Experiment Video

Updated: Jul 8, 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

20-hydroxyeicosatetraenoic acid causes endothelial dysfunction via eNOS uncoupling.

Jennifer Cheng1, Jing-Song Ou, Harpreet Singh

  • 1Department of Pharmacology, New York Medical College, Valhalla, NY 10595, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|December 25, 2007
PubMed
Summary

Increased 20-hydroxyeicosatetraenoic acid (20-HETE) impairs endothelial nitric oxide (NO) production by disrupting endothelial nitric oxide synthase (eNOS) and heat shock protein 90 (HSP90) interaction, leading to endothelial dysfunction.

More Related Videos

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
08:58

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries

Published on: February 25, 2016

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
06:35

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test

Published on: April 27, 2016

Related Experiment Videos

Last Updated: Jul 8, 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

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
08:58

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries

Published on: February 25, 2016

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
06:35

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test

Published on: April 27, 2016

Area of Science:

  • Cardiovascular Biology
  • Endothelial Function
  • Vascular Physiology

Background:

  • Endothelial dysfunction, marked by reduced nitric oxide (NO) bioavailability, underlies hypertension and vascular disease.
  • Vascular cytochrome P-450 (CYP) 4A overexpression elevates 20-hydroxyeicosatetraenoic acid (20-HETE), a vasoconstrictor, contributing to endothelial dysfunction.
  • The precise mechanisms linking 20-HETE to endothelial dysfunction require further elucidation, particularly its interaction with the endothelial nitric oxide synthase (eNOS)-NO pathway.

Purpose of the Study:

  • To investigate the in vitro and in vivo cellular mechanisms by which 20-HETE interacts with the eNOS-NO system.
  • To determine if 20-HETE affects eNOS activity, NO production, or superoxide generation.
  • To explore the role of 20-HETE in modulating the association between eNOS and heat shock protein 90 (HSP90).

Main Methods:

  • In vitro studies involved treating endothelial cells with 20-HETE and measuring NO release, superoxide production, and eNOS/HSP90 interactions.
  • Specific eicosanoids (19-HETE, 19(R)-HETE) were used to assess the specificity of 20-HETE effects.
  • In vivo experiments examined acetylcholine-induced relaxation in rat arteries overexpressing CYP4A, assessing NO bioavailability markers and the impact of inhibiting 20-HETE synthesis.

Main Results:

  • 20-HETE significantly reduced calcium ionophore-stimulated NO release and increased superoxide production in endothelial cells, suggesting eNOS uncoupling.
  • The effects of 20-HETE were specific, as 19-HETE had no impact, and 19(R)-HETE competitively antagonized 20-HETE's action.
  • 20-HETE inhibited the association of eNOS with HSP90, a critical interaction for eNOS activation, and reduced phosphorylated vasodilator-stimulated phosphoprotein in vivo.

Conclusions:

  • Increased 20-HETE production, driven by CYP4A overexpression, directly impairs endothelial function by inhibiting eNOS activity.
  • The mechanism involves 20-HETE disrupting the eNOS-HSP90 interaction, leading to reduced NO bioavailability and increased superoxide production.
  • Targeting 20-HETE synthesis or action may represent a therapeutic strategy for endothelial dysfunction associated with hypertension.