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

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

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...
Formation of the Platelet Plug01:22

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...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Structure and Function of Platelets01:18

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...
Inflammation01:38

Inflammation

Overview
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...

You might also read

Related Articles

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

Sort by
Same author

Proteins of Crustacean Exoskeletons: I. Similarities and Differences among Proteins of the Four Exoskeletal Layers of Four Brachyurans.

The Biological bulletin·2018
Same author

Management of concomitant factor VII deficiency and Factor V Leiden mutation.

International journal of laboratory hematology·2017
Same author

During warfarin induction, the Fiix-prothrombin time reflects the anticoagulation level better than the standard prothrombin time.

Journal of thrombosis and haemostasis : JTH·2016
Same author

Fiix-prothrombin time monitoring improves warfarin anticoagulation outcome in atrial fibrillation: a systematic review of randomized trials comparing Fiix-warfarin or direct oral anticoagulants to standard PT-warfarin.

International journal of laboratory hematology·2016
Same author

A single test to assay warfarin, dabigatran, rivaroxaban, apixaban, unfractionated heparin, and enoxaparin in plasma.

Journal of thrombosis and haemostasis : JTH·2016
Same author

ABO-immune complex formation and impact on platelet function, red cell structural integrity and haemostasis: an in vitro model of ABO non-identical transfusion.

Vox sanguinis·2015

Related Experiment Video

Updated: Jul 7, 2026

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader
07:13

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

The PPAR-Platelet Connection: Modulators of Inflammation and Potential Cardiovascular Effects.

S L Spinelli1, J J O'Brien, S Bancos

  • 1Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 608, Rochester,NY 14642,USA.

PPAR Research
|February 22, 2008
PubMed
Summary

Platelets, key in inflammation and immunity, express peroxisome proliferator-activated receptors (PPARs). PPAR agonists reduce platelet activation, offering potential new therapies for cardiovascular disease.

More Related Videos

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry
08:04

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry

Published on: June 10, 2025

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
12:50

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

Related Experiment Videos

Last Updated: Jul 7, 2026

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader
07:13

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry
08:04

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry

Published on: June 10, 2025

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
12:50

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Pharmacology

Background:

  • Platelets, traditionally known for hemostasis and thrombosis, are increasingly recognized as critical mediators of inflammation and immune responses.
  • Vascular inflammation and thrombosis are closely linked, with activated platelets playing a significant role in the progression of cardiovascular disease (CVD).
  • Peroxisome proliferator-activated receptors (PPARs), crucial regulators of inflammation, have been identified within platelets.

Purpose of the Study:

  • To investigate the role of platelet PPARs in modulating platelet activation and inflammatory mediator release.
  • To explore the therapeutic potential of PPAR agonists in managing platelet-driven inflammation and CVD.

Main Methods:

  • Identification and characterization of PPAR subtypes (PPARbeta/delta and PPARgamma) in human platelets.
  • Assessment of the effects of PPAR agonists on platelet activation markers and the release of inflammatory mediators like CD40 ligand (CD40L).

Main Results:

  • PPARs (PPARbeta/delta and PPARgamma) were confirmed to be present in platelets.
  • PPAR agonists were shown to effectively attenuate platelet activation.
  • This attenuation is associated with reduced release of pro-inflammatory mediators, such as CD40 ligand (CD40L).

Conclusions:

  • Platelet PPARs represent a significant target for modulating platelet activity and inflammation.
  • PPAR agonists demonstrate therapeutic promise for cardiovascular disease by dampening platelet-driven inflammatory cascades.
  • Further research into the mechanisms of platelet PPARs can inform the development of novel, safer CVD treatments.