Platelets have no nucleus: they are fragments of cytoplasm which are derived from the megakaryocytes of the bone marrow, and then enter the circulation. These unactivated platelets are biconvex discoid structures shaped like a lens, 2–3 µm in greatest diameter.
Platelets are found only in mammals, an adaptation that may have evolved to offset the risk of death from hemorrhage at childbirth – a risk unique to mammals.
see platelet count.
Platelets are not only the smallest blood cell, they are the lightest. Therefore they are pushed out from the center of flowing blood to the wall of the blood vessel. There they roll along the surface of the vessel wall, which is lined by cells called endothelium. The endothelium is a very special surface, like Teflon, that prevents anything from sticking to it. However when there is an injury or cut, and the endothelial layer is broken, the tough fibers that surround a blood vessel are exposed to the liquid flowing blood. It is the platelets that react first to injury. The tough fibers surrounding the vessel wall, like an envelop, attract platelets like a magnet, stimulate the shape change that is shown in the pictures above, and platelets then clump onto these fibers, providing the initial seal to prevent bleeding, the leak of red blood cells and plasma through the vessel injury.
Diagnostic platforms providing biomarkers that are highly predictive for diagnosing, monitoring, and stratifying cancer patients are key instruments in the development of personalized medicine.
Nilsson et al., demonstrate that tumor cells transfer (mutant) RNA into blood platelets in vitro and in vivo, and show that blood platelets isolated from glioma and prostate cancer patients contain the cancer-associated RNA biomarkers EGFRvIII and PCA3, respectively. In addition, gene-expression profiling revealed a distinct RNA signature in platelets from glioma patients compared with normal control subjects. Because platelets are easily accessible and isolated, they may form an attractive platform for the companion diagnostics of cancer 1).
Different cells appear to act as triggers of the aberrant angiogenesis, and, among them, platelets act as key participants.
In order to provide further insights into the platelet features and angiogenic role in GBM, this study investigated the effects of platelet releasate on GBM-derived endothelial cells (GECs) and the levels of VEGF and endostatin, as pro- and anti-angiogenic components of platelet releasate from GBM patients. We demonstrate for the first time that: 1) platelet releasate exerts powerful pro-angiogenic effect on GECs, suggesting it might exert a role in the aberrant angiogenesis of GBM; 2) ADP and thrombin stimulation leads to significantly higher level of VEGF, but not of endostatin, in the releasate of platelets from GBM patients than those from healthy subjects; and 3) the intraplatelet concentrations of VEGF were significantly elevated in GBM patients as compared to controls. Moreover, we found a direct correlation between platelet-released VEGF and overall survival in our patient cohort. Although preliminary, these findings prompt further investigations to clarify the biologic relevance of platelet VEGF in GBM and prospective studies for screening GBM patients for anti-VEGF therapy and/or to optimize this treatment 2).