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PRP in Vitiligo
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
PRP contains various growth factors contained in alpha granules and dense granules of platelets. Alpha granules contain various growth factors as platelet-derived growth factors (PDGFaa, PDGFbb, and PDGFab), transforming growth factor beta (TGFb1 and 2), epithelial growth factor (EGF), and vascular endothelial growth factor (VEGF) [4]. In an analysis of PRP prepared from 10 healthy individuals, in comparison to the whole blood as compared with platelet-rich plasma, the platelet-derived growth factor-BB concentration increased from 3.3 +/− 0.9 ng/mL to 17 +/− 8 ng/mL, TGFb1 concentration increased from 35 +/− 8 ng/mL to 120 +/− 42 ng/mL, VEGF concentration increased from 155 +/− 110 pg/mL to 955 +/− 1030 pg/mL, and EGF concentration increased from 129 +/− 61 pg/mL to 470 +/− 320 pg/mL [5].
Congenital Platelet Dysfunction and von Willebrand Disease
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
A selective deficiency of platelet alpha granules, in which patients have platelets that are deficient in their cellular content of platelet fibrinogen, platelet factor 4, β-thromboglobulin, and platelet-derived growth factor, has also been described. Due to the appearance of these large platelets on peripheral blood films, this disorder is known as the gray platelet syndrome. Platelet function is abnormal with respect to both aggregation and secretion.
Platelet Disorders Douglas Triplett
Published in Genesio Murano, Rodger L. Bick, Basic Concepts of Hemostasis and Thrombosis, 2019
The deficiency of the storage pool ADP explains the abnormalities seen in the aggregation response. In addition to being deficient in ADP, the platelets of patients with storage pool disease will also have decreased amounts of serotonin and calcium.111 By electron microscopy, the number of visible dense bodies is markedly diminished, while the number of alpha granules is within normal limits.106 The exact nature of the defect has not been elucidated. However, an animal model has recently become available. This inbred strain of rat (the Fawn-hooded strain) has the characteristic findings of storage pool deficiency, and it has been noted that the content of the dense bodies is deficient even in young platelets that are being fragmented from the megakaryocytic cytoplasm. Thus the disorder appears to be one of an abnormal thrombopoiesis with decreased incorporation of ADP into the platelet at the time of production. One other interesting aspect of this animal model is the bizarre behavior these rats frequently exhibit.
Innate immune TLR7 signaling mediates platelet activation and platelet-leukocyte aggregate formation in murine bacterial sepsis
Published in Platelets, 2022
Brittney Williams, Jing Zhu, Lin Zou, Wei Chao
We have previously demonstrated [6] that sepsis-induced thrombocytopenia, systemic inflammation, and coagulopathy were partly attributable to TLR7, a single-stranded RNA sensor [7–9]. However, the mechanism by which TLR7 signaling mediates platelet activation and thrombocytopenia in bacterial sepsis remains unknown. Platelet alpha granules contain up to 300 different types of proteins and polypeptides, which serve to supplement thrombin generation and mediate inflammation [10]. Platelet activation and alpha degranulation will lead to the translocation of CD62P (P-selectin), a cell adhesion molecule, to the platelet membrane to facilitate platelet-leukocyte aggregate (PLA) formation [10]. This is followed by a rapid sequestration of activated platelets from circulation and contributes to thrombocytopenia [5,11]. In the current study, we tested the hypothesis that TLR7 stimulation is sufficient to induce platelet activation and mediates PLA formation during bacterial sepsis.
Prevalence and natural history of variants in the ANKRD26 gene: a short review and update of reported cases
Published in Platelets, 2022
Hrushikesh Vyas, Ahmad Alcheikh, Gillian Lowe, William S Stevenson, Neil V Morgan, David J Rabbolini
Patients with ANKRD26-RT typically have lifelong mild (100–150 x109 cells/L) to moderate (50–99 x109 cells/L) thrombocytopenia, although counts may temporarily normalize in response to infection or inflammation [5,15]. The bleeding phenotype is variable. Most have a normal or mild bleeding phenotype without a history of spontaneous or prolonged surgical bleeding [7,16]. However, some individuals experiencing spontaneous epistaxis, bruising, or menorrhagia have also been reported. Morphologically, platelets appear normal in size and mean platelet volume is usually within normal range. Under light microscopy, platelets appear predominantly normogranular, with occasional hypogranular forms noted in some individuals. By electron microscopy, a reduction in alpha-granules has been described, as well as, increased particulate proteasome-rich cytoplasmic structures, the cause of which is yet to be clarified [16,17]. Platelet aggregation studies are often normal, however, reduced platelet responses to arachidonic acid and epinephrine have been reported. GPIa is commonly reduced when evaluated by flow cytometry and up to a sevenfold increase in serum thrombopoietin levels is seen in some cases [10,11,16]. Dysmegakaryopoiesis with an increase in small and hypolobulated megakaryocytes with reduced cytoplasmic volume is commonly cited in those who have undergone bone marrow biopsies [11,18]. Hemoglobin and white cell counts are generally within the normal range, with inconsistent reports of leukocytosis and erythrocytosis described [10,19].
Loss of mDia1 and Fhod1 impacts platelet formation but not platelet function
Published in Platelets, 2021
Malou Zuidscherwoude, Elizabeth J. Haining, Victoria A. Simms, Stephanie Watson, Beata Grygielska, Alex T. Hardy, Andrea Bacon, Stephen P. Watson, Steven G. Thomas
Increased GPIbα expression on platelets might also be expected to enhance initial binding to Von Willebrand factor upon exposure to collagen. However, in vitro flow experiments of whole blood over collagen-coated chambers indicated no significant effect of this increased GPIbα on aggregate formation (Table I and Supp. . 8). Whether this small increase in GPIbα is sufficient to cause reduced time to clot in vivo, is unclear. Furthermore, increased expression of P-selectin on resting platelets from mDia1 KO and DKO mice might indicate enhanced alpha granule secretion; indeed P-selectin expression in activated platelets was increased in these mice; however, this was not significantly different to WT. Enhanced alpha granule secretion would lead to enhanced release of pro-thrombotic and pro-inflammatory mediators leading to the formation of platelet micro-aggregates or platelet-leukocyte, monocyte, and neutrophil aggregates and increased thrombotic risk. However, we did not test the levels of these factors directly in our mice.