Related Experiment Video
Updated: May 11, 2026
10:10
Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
Published on: October 27, 2009
Histone induced platelet aggregation is inhibited by normal albumin
Fong W Lam1, Miguel A Cruz, Hon-Chiu E Leung
1Department of Pediatrics, Critical Care Section, Baylor College of Medicine, Houston, TX, USA. flam@bcm.edu flam@bcm.edu
Thrombosis Research
|May 16, 2013
Summary
Albumin prevents extracellular histones from causing platelet aggregation, a key factor in sepsis. This protective effect is charge-dependent, highlighting albumin's role in mitigating histone-induced thrombosis.
Area of Science:
- Biochemistry
- Hematology
- Immunology
Background:
- Extracellular histones, including histone H4, are implicated in sepsis pathogenesis.
- Histones promote platelet aggregation and thrombosis during inflammation and cell death.
- Mechanisms protecting against circulating histones are not fully understood.
Purpose of the Study:
- To investigate the role of albumin in preventing histone-induced platelet activation.
- To test the hypothesis that albumin inhibits histone effects on platelets.
Main Methods:
- Optical aggregometry and flow cytometry were used to assess platelet aggregation.
- Human plasma and serum albumin were tested for their effects on histone H4-induced platelet aggregation.
- Albumin was depleted from plasma and its surface charge modified to evaluate its inhibitory function.
Main Results:
- Histone H4 dose-dependently induced platelet aggregation.
- Plasma and human serum albumin inhibited histone-induced aggregation in a dose-dependent manner.
- Albumin depletion reduced plasma's inhibitory capacity, and surface neutralization of albumin impaired its function.
Conclusions:
- Normal albumin inhibits histone-induced platelet aggregation.
- This inhibition is dependent on albumin's charge.
- Albumin plays a protective role against histone-mediated platelet activation and thrombosis.
Related Concept Videos
01:22Formation 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...
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...
01:20Antiplatelet 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...
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
01:29Drug Distribution: Plasma Protein Binding
Drugs predominantly attach to plasma proteins, with only a small percentage remaining unbound. The unbound portion can be calculated as one minus the bound fraction. Acidic drugs form large, inactive complexes by reversibly binding to plasma albumin, which prevents them from diffusing across biological barriers. These drug-protein complexes act as reservoirs for the drugs. As the concentration of unbound drugs decreases, these complexes quickly dissociate to release the free drug, maintaining...
01:18Structure 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...
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...
01:05Introduction to Hemostasis
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, and...
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, and...