10 Steps Surrounding Platelet Activation

10-Step Platelet Activation Process

As you may already know, platelets form a significant portion of the blood. The three cells that constitute the blood are red blood cells, white blood cells and platelets. Among the three, the platelets act as the main agent for blood clotting in response to bleeding.

Platelets play a significant part in blood coagulation. The human body is sensitive to changes in platelet levels but there can be certain situations where thrombocyte or platelet count either increases or decreases.

The platelets are primarily formed out of megakaryocytes. Megakaryocyte plays an important role in blood cell formation as the parent cell that yields platelets. These precursors of blood platelets are found in the bone marrow where platelets initially accumulate and released into the bloodstream.

Megakaryocytes account for about 0.05 to 0.1 % of all the nucleated cells in the bone marrow. As the megakaryocytes develop into bigger cells, it undergoes fragmentation where 1,000 platelets are released per megakaryocyte. However, there are factors needed for normal platelet activation and function.

Thrombopoietin is the dominant hormone that controls megakaryocyte development. It has been established in a number of researches that in the presence of certain medical disorders, megakaryocytes and platelet production can be altered. This can result to either an increase or decrease in the amount of platelets in the blood.


Summary of the systematized process that takes place during platelet activation and formation.

A simplified account of the process can be summarized in the following steps, from formation to activation.

1. Formation:

Blood platelets are formed out of megakaryocytes that underwent a fragmentation process. They circulate in the bloodstream for just around 10 days.

Blood platelets are only cell fragments devoid of nucleus. Platelets may certainly don’t have nucleus, but consists of organelles that help hold the blood component in inactive form and shape.

2. Role of prostacyclin:

Blood platelets are kept in the inactive form under the inhibition of prostacyclin. The prostacyclin is a prostaglandin that prevents the formation of platelet plug, a process involved in primary hemostasis. This is also known to be an effective vasodilator.

In the presence of blood vessel injury, platelets migrate to the breakage and mixes with the endothelium. The endothelium helps trigger the activation of platelets.

3. Trigger by thromboxane:

The thromboxane is another factor along with ADP that helps trigger the growth and activation of platelets. It is a vasoconstrictor and a potent hypertensive agent.

Thromboxane triggers platelet aggregation, an important role in blood clot formation.

4. Granule Exocytosis (secretion):

When the platelets are activated by triggering agents like thromboxane, ADP etc., the contents of the granules (alpha granules, lambda granules, and dense granules) contained in the platelets will be secreted.

5. Thromboxane A2 formation:

The next step is the secretion of thromboxane A2 by activated platelets. Thromboxane A2 production eventually increases to stimulate activation of other platelets. It is also a powerful mediator for platelet aggregation response.

The thromboxane A2 is one of the most important stimuli that triggers conversion of platelets to the active form. It also leads to vasoconstriction which is important during tissue injury and inflammation.

6. Change in shape (Morphological Changes):

After the completion of previous steps starting from the formation of platelets to successfully being triggered by several stimuli for activation, changes in shape from inactive to the activated form takes place.

The original inactive shape of platelets is described as amorphous or disc-like colorless cell fragment. But when activation takes place, it makes an even more prominent shape, where it looks like spiculated spheres with several protruding extensions.

7. Binding:

Next to platelet activation is the bindings. The binding is a process that follows the change in shape where platelets clump or bind to each other, working with the common goal of forming a blood clot. The binding results to platelet plug formation.

The binding is mainly achieved with the use of receptors. The receptors are found in the outer layer of the activated platelets. The fibrinogen, a soluble protein and coagulation factor, is a substance that binds to its receptor in the process of clumping together.

The process involves the release of the alpha granules that contains several clotting mediators.

8. Blood coagulation:

Blood coagulation is the process where the blood changes from liquid to gel in response to bleeding. When platelets successfully take an activated form and clumped together, it forms a blood clot. This results to hemostasis, the cessation of blood loss in the damaged blood vessel.

Primary hemostasis happens when platelets immediately form a plug at the site of injury.

Secondary hemostasis happens when it does it simultaneously.

The coagulation process involves a mechanism of activation, adhesion, and aggregation of platelets. Moreover, there are several coagulation factors or clotting factors that respond in a complex cascade for the formation of fibrin strands that strengthens the platelet plug.

9. Conversion of inactive blood protein to enzyme:

Along with the mechanisms initiated by platelets, blood-clotting proteins that circulate in the blood plasma are poised to participate in blood coagulation in response to the tissue injury.

These inactive proteins become converted to active proteolytic enzymes.

10. Conversion of Prothombin to Thrombin:

The next and final step is the conversion of prothombin to the active enzyme thrombin. The sequence is dependent on the platelet response.

In combination with platelets, it completes the blood clot. The enzyme converts the blood protein fibrinogen, which is also present in plasma, to fibrin. The resulting fibrin molecules adhere to each other and assemble long fibrils. As the developing fibrils of fibrin is formed, interspersed activated platelets are trapped, forming the clot.

Key Takeaway:

Identifying the steps that surround the platelet activation process, you’ll find that each and every step, is influenced by several factors.

It’s clear that the entire process can only be completed with the presence of mutual help between one factor to another. Blood platelets, prothrombin, regulatory membrane, blood proteins, active enzyme transformations, etc. work together in a cooperative fashion towards the common goal of stopping the bleeding.

The importance of keeping the entire process functional should always be highly considered, knowing that the inability to stop bleeding can result to a life-threatening condition.

Platelet count can be altered by several factors resulting to abnormal levels. These may either be factors that cause a low platelet count or high platelet count, or it may simply be a mild drop in platelets during pregnancy.

Whatever the reason, if you’ve noticed any unusual changes in platelet count levels, take into account undergoing diagnostic procedures to identify any possible abnormalities.


Updated: October 6, 2018

About the Author:

Melissa Gomez, RN, MSN is a board certified nurse and has been a contributing writer for the past five years. Ms. Gomez has a special focus on platelet-related illness prevention and health promotion.

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