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

Formation of the Platelet Plug

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...

Structure and Function of Platelets

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...

Redox Reactions

Redox Reactions

Redox reactions are vital biochemical processes that underpin energy metabolism in cells. These reactions involve the transfer of electrons between molecules, occurring in tandem as oxidation and reduction. Oxidation refers to the loss of electrons, while reduction denotes their gain. This coupling ensures the seamless flow of electrons through metabolic pathways. For example, in bacterial metabolism, glucose undergoes oxidation to carbon dioxide, while oxygen is simultaneously reduced to...

Redox Reactions

Redox Reactions

Oxidation-reduction or redox reactions involve the transfer of electrons from one molecule or atom to another. When an atom gains an electron, another atom must lose an electron, meaning oxidation and reduction must occur together. Since the redox occurs in pairs, the atom that gets oxidized is also called the reducing agent or reductant, and the atom that is reduced is also called the oxidizing agent or oxidant. A straightforward way to remember the definitions of oxidation and reduction is...

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...

You might also read

Related Articles

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

Sort by

Same author

Oxidized PDI promotes thrombus formation in oxidative stress.

Blood·2026

Same author

Thioredoxin-related transmembrane protein 1 negatively regulates coagulation and phosphatidylserine exposure.

Research and practice in thrombosis and haemostasis·2024

Same author

Recent advances in vascular thiol isomerases and redox systems in platelet function and thrombosis.

Journal of thrombosis and haemostasis : JTH·2024

Same author

Protein disulfide isomerase A1 as a novel redox sensor in VEGFR2 signaling and angiogenesis.

Angiogenesis·2022

Same author

A novel role for endoplasmic reticulum protein 46 (ERp46) in platelet function and arterial thrombosis in mice.

Blood·2021

Same author

Vascular thiol isomerases in thrombosis: The yin and yang.

Journal of thrombosis and haemostasis : JTH·2020

Search research articles

Related Experiment Video

Updated: Jun 27, 2026

Alternative Methods for the Detection of Superoxide Anion Generation in Platelets

Alternative Methods for the Detection of Superoxide Anion Generation in Platelets

Published on: March 29, 2024

Redox control of platelet function.

David W Essex¹

¹Department of Medicine and the Sol Sherry Thrombosis Research Center, Philadelphia, Pennsylvania 19140, USA. david.essex@temple.edu

Antioxidants & Redox Signaling

|December 9, 2008

Summary

This summary is machine-generated.

Redox biology research reveals that thiols are crucial for controlling platelet function. Understanding extracellular thiol-redox states may offer new therapeutic targets for diseases.

More Related Videos

Microfluidics in Assessing Platelet Function

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

Related Experiment Videos

Last Updated: Jun 27, 2026

Alternative Methods for the Detection of Superoxide Anion Generation in Platelets

Alternative Methods for the Detection of Superoxide Anion Generation in Platelets

Published on: March 29, 2024

Microfluidics in Assessing Platelet Function

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

Area of Science:

Redox biology
Platelet physiology
Extracellular matrix interactions

Background:

Thiol-based redox reactions are central to biological control mechanisms.
Platelet function, particularly receptor activation, relies on specific thiol chemistry.
Extracellular proteins and receptors on platelets are subject to redox regulation.

Purpose of the Study:

To explore the role of thiols and redox biology in regulating platelet function.
To investigate the enzymatic control of platelet receptors, such as alphaIIbbeta3.
To understand how extracellular redox state influences platelet activity and potential therapeutic strategies.

Main Methods:

Analysis of thiol-based reactions in platelet proteins.
Investigation of enzymatic control, including protein disulfide isomerase, in receptor activation.
Examination of the effects of low molecular weight thiols, nitric oxide, and reactive oxygen species on platelet function.

Main Results:

Free thiols in the alphaIIbbeta3 fibrinogen receptor are essential for its activation.
Protein disulfide isomerase enzymatically regulates the activation of alphaIIbbeta3 and alpha2beta1 integrins.
Low molecular weight thiols modulate redox-sensitive disulfide bonds and maintain redox potential.
Nitric oxide and reactive oxygen species differentially regulate platelet responses.
Nitrosative or oxidative modifications of platelet thiols can alter platelet function.

Conclusions:

Thiol-dependent redox reactions are critical regulators of platelet activation and function.
The extracellular redox environment significantly impacts platelet behavior in health and disease.
Modulation of extracellular thiols and redox state presents a potential therapeutic avenue for managing platelet-related disorders.