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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...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
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.
Coagulation01:09

Coagulation

The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
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Introduction to Hemostasis

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Updated: Jun 7, 2026

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
10:10

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Published on: October 27, 2009

The Fluid-phase SC5b-9 Terminal Complement Complex Binds to the GPIIb/IIIa Complex of Thrombin-stimulated Human Blood

M Røger1, K Høgåsen, P A Holme

  • 1Institute of Pathology, Rikshospitalet, N-0027, Oslo.

Platelets
|November 4, 2010
PubMed
Summary

The terminal complement complex SC5b-9 interacts with human platelets via GPIIb/IIIa, inhibiting aggregation. This study reveals a novel biological role for SC5b-9 in platelet function.

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Last Updated: Jun 7, 2026

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
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Published on: October 27, 2009

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

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Area of Science:

  • Immunology
  • Hematology
  • Biochemistry

Background:

  • The terminal complement complex SC5b-9 is a non-cytolytic variant of the membrane attack complex.
  • Platelets play crucial roles in hemostasis, thrombosis, and inflammation.
  • Interactions between complement proteins and platelets can significantly impact immune responses and vascular health.

Purpose of the Study:

  • To investigate the interactions between human blood platelets and the fluid-phase terminal complement complex SC5b-9.
  • To elucidate the functional consequences of SC5b-9 binding to platelets.
  • To identify the specific platelet receptors involved in SC5b-9 interaction.

Main Methods:

  • Crossed radio-immunoelectrophoresis to assess SC5b-9 affinity for platelet glycoprotein IIb/IIIa (GPIIb/IIIa).
  • Enzyme immunoassay (EIA) to study platelet adhesion to SC5b-9 coated surfaces.
  • Dual-channel aggregometry and electron microscopy to evaluate the effect of SC5b-9 on platelet aggregation.

Main Results:

  • SC5b-9 demonstrated affinity for platelet GPIIb/IIIa, suggesting a specific binding interaction.
  • Thrombin-stimulated platelets adhered to SC5b-9 coated surfaces, an interaction inhibited by RGDS peptide, indicating involvement of the RGD sequence.
  • SC5b-9 dose-dependently inhibited ADP- and thrombin-induced platelet aggregation, with platelets showing activation and secretion but no aggregation.

Conclusions:

  • SC5b-9 interacts with human platelets through the GPIIb/IIIa complex, likely via an RGD sequence within SC5b-9.
  • SC5b-9 inhibits platelet aggregation, suggesting a regulatory role in platelet activation.
  • This study reports the first evidence of a biological role for the SC5b-9 complex in modulating platelet function.