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

Coagulation01:06

Coagulation

1.3K
Colloidal solids are solid particles suspended in solution. They are usually negatively charged, attracting a compact primary layer of positively charged ions, which attract more counterions to form an electrical double layer. Electrostatic repulsion between the charged double layers prevents the particles from colliding, stabilizing the colloids. These solids are often undesirable because they can contain toxins that are difficult to remove. Coagulation is a technique that helps aggregate and...
1.3K
Coagulation01:09

Coagulation

9.8K
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...
9.8K
Factors Affecting Activity Coefficient01:17

Factors Affecting Activity Coefficient

1.5K
The extended Debye-Hückel equation indicates that the activity coefficient of an ion in an aqueous solution at 25°C depends on three partially interdependent properties: the ionic strength of the solution, the charge of the ion, and the ion size. 
The activity coefficient value for an ion is close to one when the solution has almost zero ionic strength, i.e., when the solution shows close to ideal behavior. As the ionic strength of the solution increases from 0 to 0.1 mol/L, a...
1.5K
Transcription Factors02:16

Transcription Factors

82.3K
Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
82.3K
Cholesterol: Significance and Regulation01:29

Cholesterol: Significance and Regulation

1.3K
Although not a source of energy, cholesterol plays a significant role as a foundational structure for bile salts, steroid hormones, and vitamin D, as well as being a crucial component of plasma membranes. Approximately 15% of blood cholesterol is derived from our diet, with the remainder synthesized from acetyl CoA by the liver and intestines. Cholesterol is eliminated from the body through its conversion into bile salts, which are eventually discarded in the feces.
Considering cholesterol and...
1.3K
Complement System01:27

Complement System

9.9K
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...
9.9K

You might also read

Related Articles

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

Sort by
Same author

Structural basis of complement anaphylatoxin receptor activation by an immunostimulant lead candidate.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

In vivo evidence of effective complement modulation by TriFu in comparison to C5 inhibition and complement depletion.

Blood advances·2026
Same author

Validation of the Vision Impairment Screening Assessment in acute stroke care: a prospective diagnostic accuracy study.

European stroke journal·2026
Same author

Implantation of a Continuous-Flow Left Ventricular Assist Device During Cardiopulmonary Bypass Is Associated with a Significant and Transient Acute Thromboinflammatory Response.

International journal of molecular sciences·2026
Same author

New Analogs of the Compstatin Family of Clinical Complement Inhibitors with Low Picomolar Target Affinity.

Journal of medicinal chemistry·2026
Same author

Effect of Interleukin-6 Receptor Inhibition by Tocilizumab on Platelet Activation and Markers of Thrombus Formation: A Substudy of the ASSAIL-MI Trial.

Arteriosclerosis, thrombosis, and vascular biology·2026

Related Experiment Video

Updated: Jan 22, 2026

Enrichment of Mammalian Tissues and Xenopus Oocytes with Cholesterol
10:12

Enrichment of Mammalian Tissues and Xenopus Oocytes with Cholesterol

Published on: March 25, 2020

6.6K

Cholesterol Crystals Induce Coagulation Activation through Complement-Dependent Expression of Monocytic Tissue

Caroline S Gravastrand1,2, Bjørg Steinkjer1,2, Bente Halvorsen3,4,5

  • 1Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, 7491 Trondheim, Norway.

Journal of Immunology (Baltimore, Md. : 1950)
|July 5, 2019
PubMed
Summary

Cholesterol crystals activate complement, leading to monocyte tissue factor expression and thrombosis. Inhibiting complement C5aR1 significantly reduces this effect, highlighting a key pathway in blood clot formation.

More Related Videos

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
10:57

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

Published on: January 12, 2020

11.2K
Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
06:29

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

31.1K

Related Experiment Videos

Last Updated: Jan 22, 2026

Enrichment of Mammalian Tissues and Xenopus Oocytes with Cholesterol
10:12

Enrichment of Mammalian Tissues and Xenopus Oocytes with Cholesterol

Published on: March 25, 2020

6.6K
NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
10:57

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

Published on: January 12, 2020

11.2K
Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
06:29

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

31.1K

Area of Science:

  • * Cardiovascular Biology
  • * Immunology
  • * Thrombosis Research

Background:

  • * Cholesterol crystals (CC) are known complement activators.
  • * Potential involvement of CC in thromboinflammation via complement-coagulation cross-talk is suggested.
  • * Understanding CC's role in coagulation is crucial for cardiovascular disease research.

Purpose of the Study:

  • * To investigate the coagulation-inducing potential of cholesterol crystals.
  • * To elucidate the mechanisms underlying CC-mediated prothrombotic effects.
  • * To explore the role of complement activation in CC-induced coagulation.

Main Methods:

  • * Human whole blood and plasma models with lepirudin anticoagulant.
  • * Measurement of prothrombin fragment 1+2 (PTF1.2) and tissue factor (TF) expression.
  • * Immunohistological examination of human brain thrombi and carotid atherosclerotic plaques.

Main Results:

  • * CC exposure induced time- and concentration-dependent prothrombin fragment 1+2 generation and tissue factor expression in monocytes.
  • * TF pathway blockade abolished CC-mediated coagulation; FXII inhibition showed minor effects in plasma.
  • * Complement inhibition (C3, C5, C5aR1) significantly blocked CC-induced PTF1.2 and TF+ monocytes.
  • * In vivo findings confirmed CC proximity to monocytes, TF, and complement activation in thrombi and plaques.

Conclusions:

  • * Cholesterol crystals induce monocyte tissue factor expression, contributing to thrombosis.
  • * Complement activation, particularly via C5aR1 signaling, is critical for CC-induced procoagulant activity.
  • * CC are identified as potential contributors to thrombosis through complement-mediated pathways.