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

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

11.1K
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...
11.1K
Structure and Function of Platelets01:18

Structure and Function of Platelets

7.1K
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...
7.1K
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

769
Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
769
Introduction to Hemostasis01:05

Introduction to Hemostasis

19.5K
Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized,...
19.5K
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

10.6K
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
10.6K
Disorders of Hemostasis01:24

Disorders of Hemostasis

2.9K
Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
2.9K

You might also read

Related Articles

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

Sort by
Same author

Contrasting Effects of Platelet GPVI Deletion Versus Syk Inhibition on Mouse Jugular Vein Puncture Wound Structure.

International journal of molecular sciences·2025
Same author

Enhancing Neoadjuvant Virotherapy's Effectiveness by Targeting Stroma to Improve Resectability in Pancreatic Cancer.

Biomedicines·2024
Same author

The Tumor Microenvironment and Immune Response in Breast Cancer.

International journal of molecular sciences·2024
Same author

Platelet Count and Platelet Volume in Patients with CKD.

Journal of the American Society of Nephrology : JASN·2023
Same author

Role of Histamine and Related Signaling in Kaposi's Sarcoma-Associated Herpesvirus Pathogenesis and Oncogenesis.

Viruses·2023
Same author

VT68.2: An Antibody to Chondroitin Sulfate Proteoglycan 4 (CSPG4) Displays Reactivity against a Tumor-Associated Carbohydrate Antigen.

International journal of molecular sciences·2023
Same journal

Fibrocytes drive JAK2V617F-mutated myelofibrosis: pitavastatin reverses marrow fibrosis and anemia.

Blood·2026
Same journal

Identifying steroid-refractory aGVHD before it happens.

Blood·2026
Same journal

ELISA-negative HIT: antibody recognition and relevance.

Blood·2026
Same journal

EBV and immunodeficiency: the odd couple drawn to the brain.

Blood·2026
Same journal

A bone to pick with ferric carboxymaltose.

Blood·2026
Same journal

A step toward streamlining HIT diagnosis.

Blood·2026
See all related articles

Related Experiment Video

Updated: Apr 19, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

1.9K

Platelets: balancing the septic triad.

Jerry Ware1, Steven R Post1

  • 1UNIVERSITY OF ARKANSAS FOR MEDICAL SCIENCE.

Blood
|December 16, 2014
PubMed
Summary
This summary is machine-generated.

Platelets play a dynamic role in pneumonia-induced sepsis, modulating both infection and inflammation. This study highlights their complex involvement in the immune response.

More Related Videos

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
09:38

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

Published on: February 14, 2017

14.6K
Live-cell Imaging of Platelet Degranulation and Secretion Under Flow
11:42

Live-cell Imaging of Platelet Degranulation and Secretion Under Flow

Published on: July 10, 2017

12.3K

Related Experiment Videos

Last Updated: Apr 19, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

1.9K
A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
09:38

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

Published on: February 14, 2017

14.6K
Live-cell Imaging of Platelet Degranulation and Secretion Under Flow
11:42

Live-cell Imaging of Platelet Degranulation and Secretion Under Flow

Published on: July 10, 2017

12.3K

Area of Science:

  • Hematology
  • Immunology
  • Infectious Diseases

Background:

  • Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection.
  • Pneumonia is a common cause of sepsis.
  • The role of platelets in sepsis is complex and not fully understood.

Purpose of the Study:

  • To investigate the dynamic role of platelets in a mouse model of pneumonia-derived sepsis.
  • To illustrate how platelets modulate infection and the inflammatory response during sepsis.

Main Methods:

  • Utilized a mouse model of pneumonia-induced sepsis.
  • Employed techniques to assess platelet function and interaction with immune cells.
  • Analyzed inflammatory markers and bacterial load.

Main Results:

  • Platelets were found to dynamically modulate the infection process.
  • Platelet activity influenced the host's inflammatory response.
  • Specific interactions between platelets and other immune components were identified.

Conclusions:

  • Platelets are critical modulators of the host response in pneumonia-derived sepsis.
  • Understanding platelet dynamics offers potential therapeutic targets for sepsis treatment.