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Thrombopoiesis is the formation of thrombocytes (blood platelets) in the bone marrow. Thrombopoietin is the main regulator of thrombopoiesis. Thrombopoietin affects most aspects of the production of platelets. This includes self-renewal and expansion of hematopoietic stem cells, stimulating the increase of megakaryocyte progenitor cells, and supporting these cells so they mature to become platelet-producing cells. [2] The process of Thrombopoiesis is caused by the breakdown of proplatelets (mature megakaryocyte membrane pseudopodial projections). During the process almost all of the membranes, organelles, granules, and soluble macromolecules in the cytoplasm are being consumed. Apoptosis also plays a role in the final stages of thrombopoiesis by letting proplatelet processes to occur from the cytoskeleton of actin. [3]



Platelets are formed by megakaryocytes and are present in the bloodstream for 5–7 days. Platelets are regulators of hemostasis and thrombosis. Platelets become active in the blood following vascular injury. Vascular injury causes platelets to stick to the cellular matrix that is exposed under the endothelium, form a platelet plug, and then form a thrombus. Platelets are essential in the formation of an occlusive thrombus and are the main target of preventing the formation of an arterial thrombus. Platelets are also important in innate immunity and regulating tumor growth and vessel leakage. [4]


The megakaryoblast is a platelet precursor that undergoes endomitosis to form megakaryocytes that have 8 to 64 nuclei. Megakaryocytes shed platelets into the bloodstream. β1-tubulin microtubules, which are found in megakaryocytes, facilitate this process of shedding platelets into the bloodstream. [5] Megakaryocytes are precursor cells that are highly specialized. Megakaryocytes give rise to 1,000 to 3,000 platelets. Megakaryocytes function in the process of Thrombopoiesis by producing platelets and releasing platelets into the bloodstream. [6] Megakaryocyte development is regulated mainly by thrombopoietin. IL-3, IL-6, and IL-11 also play a role in the development of megakaryocytes by working closely with thrombopoietin. [7]


Thrombopoietin is the main regulator in the process of thrombopoiesis. In the liver and renal tubular epithelial cells, thrombopoietin is constantly being produced. Platelets and platelet precursors clear and destroy the thrombopoietin that is produced so the concentration of plasma thrombopoietin levels and platelet and platelet precursor mass are inversely proportional. If there is less platelet mass present, less thrombopoietin is cleared, which causes an increase in free plasma thrombopoietin that stimulates thrombopoiesis. [5]

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<span class="mw-page-title-main">Platelet</span> Component of blood aiding in coagulation

Platelets or thrombocytes are a component of blood whose function is to react to bleeding from blood vessel injury by clumping, thereby initiating a blood clot. Platelets have no cell nucleus; they are fragments of cytoplasm derived from the megakaryocytes of the bone marrow or lung, which then enter the circulation. Platelets are found only in mammals, whereas in other vertebrates, thrombocytes circulate as intact mononuclear cells.

<span class="mw-page-title-main">Coagulation</span> Process of formation of blood clots

Coagulation, also known as clotting, is the process by which blood changes from a liquid to a gel, forming a blood clot. It potentially results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion and aggregation of platelets, as well as deposition and maturation of fibrin.

<span class="mw-page-title-main">Immune thrombocytopenic purpura</span> Medical condition with rash and bleeding risk

Immune thrombocytopenic purpura (ITP), also known as idiopathic thrombocytopenic purpura or immune thrombocytopenia, is a type of thrombocytopenic purpura characterized by a low platelet count in the absence of other causes, and accompanied by a red-purple rash called purpura. It leads to an increased risk of bleeding. ITP manifests in two distinct clinical syndromes: an acute form observed in children, and chronic conditions observed in adults. The acute form often follows an infection and typically resolves within two months, while chronic immune thrombocytopenia persists for longer than six months and its specific cause is unknown.

<span class="mw-page-title-main">Megakaryocyte</span> Type of bone marrow cell

A megakaryocyte is a large bone marrow cell with a lobated nucleus that produces blood platelets (thrombocytes), which are necessary for normal clotting. In humans, megakaryocytes usually account for 1 out of 10,000 bone marrow cells, but can increase in number nearly 10-fold during the course of certain diseases. Owing to variations in combining forms and spelling, synonyms include megalokaryocyte and megacaryocyte.

<span class="mw-page-title-main">Thrombopoietin</span> Mammalian protein found in Homo sapiens

Thrombopoietin (THPO) also known as megakaryocyte growth and development factor (MGDF) is a protein that in humans is encoded by the THPO gene.

von Willebrand factor Mammalian protein involved in blood clotting

Von Willebrand factor (VWF) is a blood glycoprotein that promotes hemostasis, specifically, platelet adhesion. It is deficient and/or defective in von Willebrand disease and is involved in many other diseases, including thrombotic thrombocytopenic purpura, Heyde's syndrome, and possibly hemolytic–uremic syndrome. Increased plasma levels in many cardiovascular, neoplastic, metabolic, and connective tissue diseases are presumed to arise from adverse changes to the endothelium, and may predict an increased risk of thrombosis.

<span class="mw-page-title-main">Essential thrombocythemia</span> Overproduction of platelets in the bone marrow

In hematology, essential thrombocythemia (ET) is a rare chronic blood cancer characterised by the overproduction of platelets (thrombocytes) by megakaryocytes in the bone marrow. It may, albeit rarely, develop into acute myeloid leukemia or myelofibrosis. It is one of the blood cancers wherein the bone marrow produces too many white or red blood cells, or platelets.

<span class="mw-page-title-main">POEMS syndrome</span> Paraneoplastic syndrome

POEMS syndrome is a rare paraneoplastic syndrome caused by a clone of aberrant plasma cells. The name POEMS is an acronym for some of the disease's major signs and symptoms, as is PEP.

Primary myelofibrosis (PMF) is a rare bone marrow blood cancer. It is classified by the World Health Organization (WHO) as a type of myeloproliferative neoplasm, a group of cancers in which there is activation and growth of mutated cells in the bone marrow. This is most often associated with a somatic mutation in the JAK2, CALR, or MPL genes. In PMF, the bony aspects of bone marrow are remodeled in a process called osteosclerosis; in addition, fibroblast secrete collagen and reticulin proteins that are collectively referred to as (fibrosis). These two pathological processes compromise the normal function of bone marrow resulting in decreased production of blood cells such as erythrocytes, granulocytes and megakaryocytes, the latter cells responsible for the production of platelets.

<span class="mw-page-title-main">P-selectin</span> Type-1 transmembrane protein

P-selectin is a type-1 transmembrane protein that in humans is encoded by the SELP gene.

Mean platelet volume (MPV) is a machine-calculated measurement of the average size of platelets found in blood and is typically included in blood tests as part of the CBC. Since the average platelet size is larger when the body is producing increased numbers of platelets, the MPV test results can be used to make inferences about platelet production in bone marrow or platelet destruction problems.

<span class="mw-page-title-main">GATA1</span> Protein-coding gene in humans

GATA-binding factor 1 or GATA-1 is the founding member of the GATA family of transcription factors. This protein is widely expressed throughout vertebrate species. In humans and mice, it is encoded by the GATA1 and Gata1 genes, respectively. These genes are located on the X chromosome in both species.

<span class="mw-page-title-main">Promegakaryocyte</span> Cell type

A promegakaryocyte is a precursor cell for a megakaryocyte. It arises from a megakaryoblast, into a promegakaryocyte and then into a megakaryocyte, which will eventually break off and become a platelet.

<span class="mw-page-title-main">Microvesicle</span> Type of extracellular vesicle

Microvesicles are a type of extracellular vesicle (EV) that are released from the cell membrane. In multicellular organisms, microvesicles and other EVs are found both in tissues and in many types of body fluids. Delimited by a phospholipid bilayer, microvesicles can be as small as the smallest EVs or as large as 1000 nm. They are considered to be larger, on average, than intracellularly-generated EVs known as exosomes. Microvesicles play a role in intercellular communication and can transport molecules such as mRNA, miRNA, and proteins between cells.

<span class="mw-page-title-main">Thrombopoietin receptor</span> Protein-coding gene in the species Homo sapiens

The thrombopoietin receptor also known as the myeloproliferative leukemia protein or CD110 is a protein that in humans is encoded by the MPL oncogene.

<span class="mw-page-title-main">SH2B3</span> Protein-coding gene in the species Homo sapiens

SH2B adapter protein 3 (SH2B3), also known as lymphocyte adapter protein (LNK), is a protein that in humans is encoded by the SH2B3 gene on chromosome 12.

<span class="mw-page-title-main">CFU-GEMM</span>

CFU-GEMM is a colony forming unit that generates myeloid cells. CFU-GEMM cells are the oligopotential progenitor cells for myeloid cells; they are thus also called common myeloid progenitor cells or myeloid stem cells. "GEMM" stands for granulocyte, erythrocyte, monocyte, megakaryocyte.

Kenneth Kaushansky, M.D., Master of the American College of Physicians (MACP) is an American medical doctor, hematologist, former editor of the medical journal Blood, and served as the dean of the Stony Brook University School of Medicine from 2010 to 2021. Prior to moving to Stony Brook, he was the Helen M. Ranney Professor, and chair of the department of medicine at University of California, San Diego School of Medicine.

Thromboregulation is the series of mechanisms in how a primary clot is regulated. These mechanisms include, competitive inhibition or negative feedback. It includes primary hemostasis, which is the process of how blood platelets adhere to the endothelium of an injured blood vessel. Platelet aggregation is fundamental to repair vascular damage and the initiation of the blood thrombus formation. The elimination of clots is also part of thromboregulation. Failure in platelet clot regulation may cause hemorrhage or thrombosis. Substances called thromboregulators control every part of these events.

The platelet plug, also known as the hemostatic plug or platelet thrombus, is an aggregation of platelets formed during early stages of hemostasis in response to one or more injuries to blood vessel walls. After platelets are recruited and begin to accumulate around the breakage, their “sticky” nature allows them to adhere to each other. This forms a platelet plug, which prevents more blood from leaving the body as well as any outside contaminants from getting in. The plug provides a temporary blockage of the break in the vasculature. As such, platelet plug formation occurs after vasoconstriction of the blood vessels but before the creation of the fibrin mesh clot, which is the more permanent solution to the injury. The result of the platelet plug formation is the coagulation of blood. It can also be referred to as primary hemostasis.


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