Thrombocytopoiesis

A platelet is a cellular component of blood that plays an important role in protecting the body from bleeding. The formation of new platelets occurs in the bone marrow and is regulated by hormones and growth factors. Violation of the platelet component of hemostasis can lead to severe bleeding that threatens human life, so it is important to understand the mechanisms of regulation of thrombocytopoiesis.

What is platelet hemostasis?

Platelet hemostasis is the process of formation and stabilization of a blood clot at the site of vessel damage through adhesion and aggregation of platelets. In the event of a vessel injury or damage, a cascade of reactions is triggered, which leads to the formation of a blood clot. The main participant in the platelet phase of hemostasis is platelet adhesion, i.e. attraction of platelets to damaged areas of the vessel wall. A few minutes after injury, platelets become activated and change their shape, which promotes their aggregation. Finally, the aggregated platelets form a fibrin matrix around the injured vessels, creating a barrier to blood and stabilizing the site of injury.

The main regulator of thrombocytosis is the nuclear factor-κB (NF-κB) gene. Activated NF-κB induces the synthesis and activation of thrombopoietin tyrosine kinase receptors, which stimulate the proliferation of megakaryocytes, platelet precursors in the bone marrow. After proliferation, megakaryocytes differentiate into platelets and exit the bone marrow into the bloodstream.

How is the process of platelet hemostasis disrupted? Impaired platelet-vascular hemostasis occurs in various diseases and conditions, such as hemoblastosis, thrombocytopenic purpura, congenital and acquired thrombocytouria and other pathologies. The main cause of disturbances in the platelet mechanisms of hemostasis in these diseases is dysfunction of the megakaryocyte and platelet series of the bone marrow.

The role of thromboplastin in the modulation of inflammatory processes

The polypeptide thromboplastin plays a key role in triggering the cascade of coagulation reactions leading to hemostasis. Activation of the blood coagulation system begins with the addition of calcium ions to factor III and IIa (thrombin), which forms a complex capable of aggregating the sulfhydryl groups of thrombomodulin and procoagulant factors. The latter complex is a modulator of platelet activity, promoting activation of GPIIb-IIIa receptors by serotonin, reducing Ca2+ levels and cell aggregation. However, some studies have shown that, under specific operating conditions, it is also able to bind to pro-inflammatory polypeptides, such as proIL-1α and IL-1β, affecting inflammatory processes in tissues [1].

The above examples show how important it is to identify the causes of impaired platelet hemostasis and the immediate use of specialized therapy, which involves correction of the quantitative and qualitative parameters of the platelet-vascular-cell link of the hematoma process.

Thrombopoiesis is a complex process that occurs in the human bone marrow and is responsible for the formation and maintenance of a sufficient number of platelets in the blood. Blood clots are necessary to stop bleeding, so disruption of thrombopoiesis processes can lead to serious consequences. In this article we will talk about how platelet formation occurs, what factors influence this process and what diseases are associated with thrombotic disorders