Related Experiment Video
Updated: Jul 20, 2026

14:14
Optimized Fibrin Gel Bead Assay for the Study of Angiogenesis
Published on: April 29, 2007
The minimum concentration of fibrinogen needed for platelet aggregation using ADP
Robert F Cornell1, Tim R Randolph
1Department of Clinical Laboratory Science, Saint Louis University Health Sciences Center, St Louis MO 63104, USA.
Summary
Platelet aggregation, essential for blood clotting, can occur even without plasma fibrinogen when stimulated by ADP. This finding challenges previous assumptions about fibrinogen
Area of Science:
- Hematology
- Biochemistry
- Platelet Physiology
Background:
- Fibrinogen is a key protein in hemostasis, crucial for platelet aggregation and clot formation.
- The precise minimum concentration of plasma fibrinogen required to initiate platelet aggregation is not fully understood.
- Adenosine diphosphate (ADP) is a potent stimulator of platelet aggregation.
Purpose of the Study:
- To determine the minimum plasma fibrinogen concentration necessary to induce platelet aggregation.
- To investigate the role of fibrinogen concentration in ADP-induced platelet aggregation in healthy individuals.
Main Methods:
- Preparation of platelet-rich plasma from healthy volunteers.
- Adjustment of plasma fibrinogen concentrations to 75, 19, 5, and 0 mg/dL using fibrinogen-free serum.
- Aggregation of platelets with adenosine diphosphate (ADP) at each fibrinogen concentration.
- Analysis of aggregation tracings for amplitude, curve type, smoothness, and stability.
Main Results:
- Platelet aggregation was observed at all tested fibrinogen concentrations, including zero.
- The amplitude of platelet aggregation curves did not appear to be dependent on plasma fibrinogen levels.
- Aggregation curves showed consistent patterns across varying fibrinogen concentrations.
Conclusions:
- Healthy platelets, even after exposure to normal fibrinogen levels, aggregate effectively with ADP across a wide range of fibrinogen concentrations.
- Plasma fibrinogen may not be essential for ADP-induced platelet aggregation in healthy individuals.
- Further research is needed to elucidate the mechanisms of fibrinogen-independent platelet aggregation.
Related Concept Videos
Intracellular Signaling Affects Focal Adhesions
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Some...
Antiplatelet 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...
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...
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...
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.

