Platelets Play a Large Role in Tissue Regeneration and Repair

In Cardone presentation, His main focus was on Platelet-rich plasma (PRP), (plasmas that come from the patient’s body, and is centrifuged to increase the concentration of platelets combined with remaining blood). He also discussed the potential advantages as well as potential drawbacks and uncertainties regarding the use of PRP injections to treat

This chronic myeloproliferative disorder (MPD) is associated with mass quantity of platelets that are put out by megakaryocytes

After the occurrence of a wound the inflammatory process immediately begins and can last up to 3 days ("Wound Healing" 2016), the initial injury causes the small vessels around the wound site to be disturbed resulting in bleeding, the body’s first response is a haemodynamic one in that it restricts these vessels in order to prevent blood loss. There then comes a rapid release of preformed inflammatory mediators from the cells surrounding the injury, the first thing this causes is the aggregation of platelets, these platelets adhere to extracellular surface structures which are exposed, such as collagen and basement membranes, this in turn causes serotonin from platelet stores to be stimulated. (Kirk, Phillips and Murray 2001)

Several studies have shown the microenvironment and ECM are reservoirs of cellular and non-cellular materials, which help, modulate growth, survival, motility and invasive behaviour (LR)(Maeda et al., 2004). Hence studies on tumour epithelial cells and their niche are of current interest, as these interactions with regards to tumorigenesis have not fully been

overproduction of megakaryocytes in the bone marrow. This means the platelets number increase in the peripheral blood and it is called Thrombocythemia. This disorder is called essential because the increase in platelets number is a distinctive problem of the blood cell production in the bone marrow (Rumi et al., 2014).

Platelets are small fragments of cells. Platelets process coagulation. This is done by them gathering at the site of an injury and in turn sticking to the lining of the injured blood vessel. This is a platform on which blood coagulations occur, resulting in the formation of a fibrin clot. This covers the wound and prevents blood from leaking out. Fibrin also forms the initial building blocks from which new tissue are formed, in- turn promoting the healing process. If there is an imbalance, for example to high of a number of platelets may result in clotting not necessary in the body that can lead to health risks or a lower than normal counts can lead to extensive bleeding. So they protect us by clotting and aiding in healing by producing

There is no fixed platelet count threshold in ICU patients that signals platelet transfusion (93), but because of hemorrhage fear there is a widespread notion that the platelet count should be maintained over 100X109/L in massive bleeding or when bleeding occurs at dangerous sites such as in intracranial hemorrhage (94).

A leading cause of death in patients with cancer, 28 thrombosis is associated with higher

The mechanisms responsible of this effect are unknown. Previous studies highlighted a relationship between the number of regulatory T-cells (T-Regs) and the status of ITP activity and response to various treatments (steroids, rituximab, TPO-R agonists) suggesting a direct effect of platelets itself in modulating the immune system, inducing a possible auto-de-sensitizing phenomenon ( 30 , 31 )

When a tissue injury occurs, platelets collect at the site and begin the clotting cycle. More importantly, these

• Cells that help the blood clot (platelets). Having too few platelets is called thrombocytopenia.

thrombocytopenia or abnormal platelet function. The time required to form a clot and for edges

with wounds that have broken through the skin, WBCs will gather around the point of entry to fight infection and prevent any further damage to systems (Tortura 699). However, in the case of hemostasis, the most important contributors are the Platelets, cell fragments that are held together with a membrane (702). As bleeding occurs, various chemicals and enzymes that are contained within platelets activate, causing the cells to become sticky and encourage accumulation to one another. This coagulation of platelets at the broken vessel’s entry site will eventually form a solid plug, resulting in effective clotting. . Clotting is essential to stop major bleeding of vessels throughout the body, especially in the case of hemorrhagic or hypovolemic shock

The ultimate location of immature hematopoietic cells is in the bone marrow. The average adult has approximately 1.7 L of bone marrow, which provides an optimal environment for the development and proliferation of hematopoietic cells. Stromal cells are thought to be important hematopoietic components, providing growth factors, collagen, and cell adhesion proteins

Activated platelets facilitate recruitment of leukocytes to regions of injury or inflammation. Platelets bind circulating leukocytes to form platelet-leukocyte aggregates in the circulation, which are subsequently recruited to the vessel wall. Initial interactions between platelet P-selectin and leukocyte PSGL-1 lead to signaling through a Src family tyrosine kinase pathway, which enhances leukocyte 2 integrin expression. [212]. Furthermore, ligation of platelet P-selectin activates IIb3 through inside-out signaling, which stabilizes platelet-leukocyte aggregate formation. These aggregates occur either in circulation or via platelet binding to the endothelial surface, and facilitate leukocyte recruitment through leukocyte 2 integrin and platelet IIb3 co-interactions with fibrinogen [213, 214][215]. In contrast, adherent neutrophils within venules have been shown to interact with P-selectin- and IIb3-expressing platelets, although a specific role for IIb3 was not identified