Sorting machineries: how platelet-dense granules differ from α-granules

Chen, Yuanying; Yuan, Yefeng; Li, Wei

doi:10.1042/bsr20180458

Cited by 48 publications

(60 citation statements)

References 78 publications

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“…It has been shown that larger platelets have denser αgranules, which store biologically active molecules such as GPIIb/IIIa, fibrinogen, and von Willebrand factor (vWf) which can initiate the coagulation cascade [30]. Dense granules store a variety of molecules which are secreted during platelet activation; including catecholamines, serotonin, calcium, adenosine 5′-diphosphate (ADP), and adenosine 5′-triphosphate (ATP) that involved in initiating coagulation cascade during inflammation [31]. Higher MPV is also seen with DIC and it has been shown that MPV plays an important role in activation of coagulation and/or hyperfibrinolysis.…”

Section: Discussionmentioning

confidence: 99%

Platelets and renal failure in the SARS-CoV-2 syndrome

et al. 2020

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The coronavirus disease 19 (COVID-19) is a highly transmittable viral infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 utilizes metallocarboxyl peptidase angiotensin receptor (ACE) 2 to gain entry into human cells. Activation of several proteases facilitates the interaction of viral spike proteins (S1) and ACE2 receptor. This leads to cleavage of host ACE2 receptors. ACE2 activity counterbalances the angiotensin II effect, its loss may lead to elevated angiotensin II levels with modulation of platelet function, size and activity. COVID-19 disease encompasses a spectrum of systemic involvement far beyond respiratory failure alone. Several features of this disease, including the etiology of acute kidney injury (AKI) and the hypercoagulable state, remain poorly understood. Here, we show that there is a high incidence of AKI (81%) in the critically ill adults with COVID-19 in the setting of elevated D-dimer, elevated ferritin, C reactive protein (CRP) and lactate dehydrogenase (LDH) levels. Strikingly, there were unique features of platelets in these patients, including larger, more granular platelets and a higher mean platelet volume (MPV). There was a significant correlation between measured D-dimer levels and MVP; but a negative correlation between MPV and glomerular filtration rates (GFR) in critically ill cohort. Our data suggest that activated platelets may play a role in renal failure and possibly hypercoagulability status in COVID19 patients.

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Section: Discussionmentioning

confidence: 99%

Platelets and renal failure in the SARS-CoV-2 syndrome

et al. 2020

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“…Upon activation, platelets release various substances from their intracellular granules that contribute to coagulation . For example, plasma PPBP and PF4 reportedly activate coagulation .…”

Section: Discussionmentioning

confidence: 99%

“…[35][36][37][38] In our splenic tissue analysis, hypothermia enhanced vWF expression in both mRNA and Upon activation, platelets release various substances from their intracellular granules that contribute to coagulation. [39][40][41][42][43][44] For example, plasma PPBP and PF4 reportedly activate coagulation. [45][46][47][48] Although we suspect that these substances were released into the plasma of hypothermic mice, we did not detect significant thrombosis or plasma D-dimer elevation in mice euthanized immediately after the hypothermia treatment.…”

Section: Discussionmentioning

confidence: 99%

Hypothermia‐induced activation of the splenic platelet pool as a risk factor for thrombotic disease in a mouse model

Horioka

Tanaka

Isozaki

et al. 2019

Journal of Thrombosis and Haemostasis

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BackgroundHypothermia, either therapeutically induced or accidental (ie, an involuntary decrease in core body temperature to <35°C), results in hemostatic disorders. However, it remains unclear whether hypothermia enhances or inhibits coagulation, especially in severe hypothermia. The present study evaluated the thrombocytic and hemostatic changes in hypothermic mice.MethodsC57Bl/6 mice were placed at an ambient temperature of −20°C under general anesthesia. When the rectal temperature decreased to 15°C, 10 mice were immediately euthanized, while another 10 mice were rewarmed, kept in normal conditions for 24 hours, and then euthanized. These treatments were also performed in 20 splenectomized mice.ResultsThe hypothermic mice had adhesion of CD62P‐positive platelets with high expression of von Willebrand factor (vWF) in their spleens, while the status of the peripheral platelets was unchanged. Furthermore, the plasma levels of platelet factor 4 (PF4) and pro‐platelet basic protein (PPBP), which are biomarkers for platelet degranulation, were significantly higher in hypothermic mice than in control mice, indicating that hypothermia activated the platelets in the splenic pool. Thus, we analyzed these biomarkers in asplenic mice. There was no increase in either PF4 or PPBP in splenectomized hypothermic mice. Additionally, the plasma D‐dimer elevation and microthrombosis were caused in rewarmed mice, but not in asplenic rewarmed mice.ConclusionsOur results indicate that hypothermia leads to platelet activation in the spleen via the upregulation of vWF, and this activation causes hypercoagulability after rewarming.

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“…Dense granules have a distinct specific cargo regarding both biogenesis and function, which contains a few types of small molecules, such as catecholamines, ADP, ATP, polyphosphate and Ca 2+ [ 38 ].…”

Section: Platelet Biology and Its Roles In Human Diseasesmentioning

confidence: 99%

Platelets in Healthy and Disease States: From Biomarkers Discovery to Drug Targets Identification by Proteomics

Gianazza

Brioschi

Baetta

et al. 2020

IJMS

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Platelets are a heterogeneous small anucleate blood cell population with a central role both in physiological haemostasis and in pathological states, spanning from thrombosis to inflammation, and cancer. Recent advances in proteomic studies provided additional important information concerning the platelet biology and the response of platelets to several pathophysiological pathways. Platelets circulate systemically and can be easily isolated from human samples, making proteomic application very interesting for characterizing the complexity of platelet functions in health and disease as well as for identifying and quantifying potential platelet proteins as biomarkers and novel antiplatelet therapeutic targets. To date, the highly dynamic protein content of platelets has been studied in resting and activated platelets, and several subproteomes have been characterized including platelet-derived microparticles, platelet granules, platelet releasates, platelet membrane proteins, and specific platelet post-translational modifications. In this review, a critical overview is provided on principal platelet proteomic studies focused on platelet biology from signaling to granules content, platelet proteome changes in several diseases, and the impact of drugs on platelet functions. Moreover, recent advances in quantitative platelet proteomics are discussed, emphasizing the importance of targeted quantification methods for more precise, robust and accurate quantification of selected proteins, which might be used as biomarkers for disease diagnosis, prognosis and therapy, and their strong clinical impact in the near future.

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Sorting machineries: how platelet-dense granules differ from α-granules

Cited by 48 publications

References 78 publications

Platelets and renal failure in the SARS-CoV-2 syndrome

Platelets and renal failure in the SARS-CoV-2 syndrome

Hypothermia‐induced activation of the splenic platelet pool as a risk factor for thrombotic disease in a mouse model

Platelets in Healthy and Disease States: From Biomarkers Discovery to Drug Targets Identification by Proteomics

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