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Related Concept Videos

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...
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...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

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.

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Related Experiment Video

Updated: May 27, 2026

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

Platelet shape change and spreading.

Joseph E Aslan1, Asako Itakura, Jacqueline M Gertz

  • 1Department of Biomedical Engineering, Department of Cell and Developmental Biology, Oregon Health & Science University, Portland, OR, USA.

Methods in Molecular Biology (Clifton, N.J.)
|December 2, 2011
PubMed
Summary
This summary is machine-generated.

Platelet activation reorganizes the actin cytoskeleton, transforming disk-shaped platelets into spread cells. This process, visualized with Nomarski microscopy, helps identify regulators of platelet function.

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Last Updated: May 27, 2026

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

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Published on: July 10, 2017

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers
05:43

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A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
04:32

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

Published on: June 5, 2019

Area of Science:

  • Hematology
  • Cell Biology
  • Biophysics

Background:

  • Hemostasis relies on platelet recruitment and activation at vascular injury sites.
  • Platelet activation involves rapid actin cytoskeleton reorganization.
  • This leads to platelet shape change from biconcave disks to spread cells.

Purpose of the Study:

  • To characterize real-time platelet morphological changes during activation.
  • To identify regulators of platelet function using advanced microscopy.

Main Methods:

  • Utilized Kohler-illuminated Nomarski Differential Interference Contrast microscopy.
  • Observed real-time morphological transformations of platelets.

Main Results:

  • Platelet activation causes significant reorganization of the cortical actin cytoskeleton.
  • Platelets transform from biconcave disks to fully spread cells.
  • Filopodia and lamellipodia extension dramatically increases platelet surface area.

Conclusions:

  • Nomarski microscopy is effective for real-time characterization of platelet shape changes.
  • This technique aids in identifying genetic and pharmacological regulators of platelet function.