Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Nitric Oxide Signaling Pathway

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...

Regulation of Angiogenesis and Blood Supply

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...

Paracrine Signaling

Paracrine Signaling

Paracrine signaling allows cells to communicate with their immediate neighbors via secretion of signaling molecules. Such a signal can only trigger a response in nearby target cells because the signal molecules degrade quickly or are inactivated if not taken up. Prominent examples of paracrine signaling include nitric oxide signaling in blood vessels, synaptic signaling of neurons, the blood clotting system, tissue repair/wound healing, and local allergic skin reactions. Nitric oxide as a...

Autoregulation of Blood Flow

Autoregulation of Blood Flow

Autoregulation mechanisms are characterized by their inherent capacity for self-regulation without necessitating specific nervous stimulation or endocrine control. These mechanisms facilitate the adjustment of blood flow and, therefore, perfusion specific to each tissue region. This self-regulation encompasses chemical signals and myogenic controls.
Chemical Signaling in Autoregulation
Chemical signaling operates at the precapillary sphincter level, inciting either contraction or relaxation.

Mechanism of Angiogenesis

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...

Structure of Blood Vessels

Structure of Blood Vessels

Blood is circulated throughout the human body through a network of blood vessels called the circulatory system. This system includes arteries that transport blood from the heart to various body parts. These arterial pathways divide into smaller vessels until they reach the arterioles, which further split into capillaries. It is within these minuscule capillaries that the exchange of nutrients and waste products takes place. After this exchange, the blood is collected by venules, which fuse to...

You might also read

Related Articles

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

Sort by

Same author

Prognostic relevance of β1-adrenergic receptor polymorphisms on cardiovascular outcome in patients treated with metoprolol after acute myocardial infarction - an observational study.

European journal of clinical pharmacology·2026

Same author

Letter from the Editor-in-Chief.

Medical science educator·2026

Same author

Letter from the Editor-in-Chief.

Medical science educator·2026

Same author

Fiber Track Length Gradients in the Avian Sound Localization Circuit Require Conduction Velocity Gradients to Maintain Isochronicity.

The Journal of comparative neurology·2026

Same author

Using design-based research to aid the development of a case-directed learning pedagogy for the preclerkship medical curriculum.

Advances in physiology education·2026

Same author

Utilization Patterns and Perceptions of a Spaced Repetition Flashcard Program, Anki, Among First-Year Medical Students.

Cureus·2025

Search research articles

Related Experiment Video

Updated: Jul 7, 2026

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Published on: June 3, 2019

Endothelial S100A1 modulates vascular function via nitric oxide.

Sven T Pleger¹, David M Harris, Changguang Shan

¹Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA.

Circulation Research

|February 23, 2008

Summary

This summary is machine-generated.

Endothelial S100A1 protein is crucial for maintaining healthy blood vessel function by regulating calcium and nitric oxide release. Its absence leads to impaired relaxation and hypertension, suggesting therapeutic potential.

More Related Videos

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000

Published on: October 15, 2010

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

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 7, 2026

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Published on: June 3, 2019

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000

Published on: October 15, 2010

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

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

Published on: April 27, 2016

Area of Science:

Cardiovascular Biology
Cellular Physiology

Background:

S100A1, a calcium-binding protein, is expressed in endothelial cells (ECs).
Intracellular calcium ([Ca2+]i) transients influence EC functions and nitric oxide synthase (NOS) activity.

Purpose of the Study:

To investigate the role of endothelial S100A1 in regulating endothelial and vascular function.
To determine the impact of S100A1 deficiency on calcium signaling and nitric oxide (NO) production in ECs.

Main Methods:

Utilized S100A1 knockout (SKO) mice and wild-type littermates.
Assessed vascular relaxation responses to acetylcholine and sodium nitroprusside in isolated thoracic aortas.
Measured basal and stimulated endothelial NO release.
Investigated intracellular calcium ([Ca2+]i) transients in ECs.
Employed siRNA to silence S100A1 expression in wild-type ECs and used S100A1 overexpression models.

Main Results:

SKO mice exhibited significantly reduced acetylcholine-induced relaxation and developed hypertension.
Endothelial NO release, both basal and stimulated, was diminished in SKO aortas.
Impaired NO production in SKO was linked to reduced agonist-induced [Ca2+]i transients in ECs.
Silencing S100A1 in wild-type ECs decreased [Ca2+]i and NO generation.
S100A1 overexpression enhanced NO generation, which was inhibited by 2-aminoethoxydiphenylborate.
Cardiac endothelial S100A1 expression was downregulated in a model of heart failure.

Conclusions:

Endothelial S100A1 critically regulates vascular function by modulating [Ca2+]i and NO release.
Lack of S100A1 contributes to impaired endothelium-dependent relaxation and hypertension.
Targeting endothelial S100A1 may offer a therapeutic strategy for vascular diseases and heart failure.