Related Experiment Video
Updated: Jul 31, 2026
11:42
Live-cell Imaging of Platelet Degranulation and Secretion Under Flow
Published on: July 10, 2017
Aspects of platelet formation and release
American Journal of Hematology
|January 1, 1981
Summary
Megakaryocytes in mouse bone marrow extend cytoplasmic processes into sinuses for platelet release. These processes may be phagocytosed by macrophages before reaching circulation, impacting platelet production.
Area of Science:
- Hematology
- Cell Biology
- Histology
Background:
- Megakaryocytes reside in the extravascular compartment of bone marrow.
- Platelet production (thrombopoiesis) is a critical hematologic process.
- Understanding megakaryocyte morphology is key to understanding platelet release.
Purpose of the Study:
- To investigate the surface architecture and location of megakaryocytes in mouse bone marrow.
- To elucidate the mechanism of cytoplasmic process extension and platelet release.
- To explore the fate of platelets released into the extravascular space.
Main Methods:
- Microscopic examination of mouse bone marrow.
- Analysis of megakaryocyte cytoplasmic processes and their interaction with sinus endothelium.
- Observation of potential platelet release and phagocytosis events.
Main Results:
- Megakaryocytes possess finger-like cytoplasmic processes extending through bone marrow sinus apertures (approx. 3.0 millimicron).
- These processes form villi, anchoring to endothelium via microfilaments, and undergo extension, attenuation, and constriction.
- Evidence suggests extravascular platelet release and subsequent phagocytosis by macrophages before entering circulation.
Conclusions:
- Megakaryocyte cytoplasmic processes play a crucial role in platelet release within the bone marrow.
- The observed morphology suggests a complex mechanism for thrombopoiesis at the cellular level.
- Phagocytosis of released platelets by macrophages may influence platelet availability in the microcirculation.
Related Concept Videos
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...
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...
01:09Coagulation
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...
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...
01:20Extrinsic 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...
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...
01:16Clot 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.