Platelets in the Newborn

Abstract

Platelets were first described in the mid-nineteenth century. Since then, their roles were identified in hemostasis and thrombosis, inflammation, leukocyte interactions, angiogenesis, and cancer growth. But there is little information about such platelet functions in the newborn. Several studies highlighted some platelet differences between newborns and adults. Yet, in spite of these differences, healthy newborns appear to be adequately protected. A number of factors, however, were reported to negatively affect neonatal platelets. These include maternal hypertensive disorders or infections, neonatal asphyxia or respiratory distress, therapies such as ampicillin or indomethacin, and treatment modalities such as ventilators, nitric oxide, or extracorporeal membrane oxygenation (ECMO). Their effects on newborn platelets are usually transitory, lasting from several hours to a few days or weeks. If these effects are well characterized, they could serve as reporters for diagnosis and monitoring during therapy. Careful studies of neonatal platelets are needed to improve the understanding of basic physiology and pathophysiology in this cohort and to identify possible targets for intervention and therapy.

Comparative Proteomics of Human Milk From Eight Cities in China During Six Months of Lactation in the Chinese Human Milk Project Study

“…Beyond its primary role in thrombus or plug formation in wound healing, the platelet also worked in tissue repair, angiogenesis, inflammation, and host defense ( 26 – 30 ). In newborns, overall platelet degranulation released during platelet activation was lower compared to adults ( 31 ). Based on our results, there was no significant difference in platelet degranulation in the 1st month across the cities ( Figure 5A ).…”

“…All proteins contributed in both terms were figured out in protein network connection ( Figure 6 ). Platelet glycoprotein 4 (CD36) had a responsibility in the phagocytosis process ( 31 ). Phagocytosis was an important innate immune response process to protect infants from microbes.…”

Impact of Reticulated Platelets on Platelet Reactivity in Neonates

“…Neonatal megakaryocytes display a developmentally distinctive uncoupling of proliferation, polyploidization, and cytoplasmic maturation, characterized by a high proliferative rate, producing large numbers of smaller size and lower ploidy megakaryocytes. 2,9 During thrombopoiesis in neonates, polyploidization enables megakaryocytes to achieve protein synthesis with large amounts of cytoplasm, and a rapid increase in the rate of platelet production in response to hemostatic demand. 4,10 The immaturity of neonatal megakaryocytes and their progenitors indicates developmental differences between neonatal and adult megakaryopoiesis 2,3 (Figure 1).…”

“…Platelets are anucleated cytoplasmic discoid-shaped cells, and their physiological role is the maintenance of vascular integrity and regulation of the hemostatic process at sites of vascular injury. 1,2 Nonactivated platelets circulate without adhering to the luminal surface of the endothelium, but in response to injury become activated, causing endothelial cell activation. 2,3 Activated platelets promote fibrin formation, recruitment of inflammatory cells to the thrombus, and initiate repair of the injured vessel wall.…”

“…1,2 Nonactivated platelets circulate without adhering to the luminal surface of the endothelium, but in response to injury become activated, causing endothelial cell activation. 2,3 Activated platelets promote fibrin formation, recruitment of inflammatory cells to the thrombus, and initiate repair of the injured vessel wall. Hemorrhage arrest depends on a set of complex regulated events; initiated by a layer of platelets adhering to a thrombogenic surface, followed by recruitment of additional platelets to the primary adhesive plug, resulting in the formation of a fibrin network of blood clot.…”