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Academic literature on the topic 'Platelet biology'

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Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Platelet biology"

Hansen, Caroline E., Yongzhi Qiu, Owen J. T. McCarty, and Wilbur A. Lam. "Platelet Mechanotransduction." Annual Review of Biomedical Engineering 20, no. 1 (June 4, 2018): 253–75. http://dx.doi.org/10.1146/annurev-bioeng-062117-121215.

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The vasculature is a dynamic environment in which blood platelets constantly survey the endothelium for sites of vessel damage. The formation of a mechanically coherent hemostatic plug to prevent blood loss relies on a coordinated series of ligand–receptor interactions governing the recruitment, activation, and aggregation of platelets. The physical biology of each step is distinct in that the recruitment of platelets depends on the mechanosensing of the platelet receptor glycoprotein Ib for the adhesive protein von Willebrand factor, whereas platelet activation and aggregation are responsive to the mechanical forces sensed at adhesive junctions between platelets and at the platelet–matrix interface. Herein we take a biophysical perspective to discuss the current understanding of platelet mechanotransduction as well as the measurement techniques used to quantify the physical biology of platelets in the context of thrombus formation under flow.

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Diamond, Scott L. "Systems Biology to Predict Platelet Function." Blood 116, no. 21 (November 19, 2010): SCI—38—SCI—38. http://dx.doi.org/10.1182/blood.v116.21.sci-38.sci-38.

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Abstract Abstract SCI-38 Systems Biology seeks to provide patient-specific prediction of dynamic cellular response to multiple stimuli, critical information toward predicting risk, disease progression, or response to therapy. We deployed two distinct approaches, bottom-up and top-down analyses, to gain insight into platelet signaling. The bottom-up approach required a definition of reaction network and kinetic equations (topology), kinetic parameters, and initial concentrations in order to simulate platelet signaling. We developed a computational platelet model – assembled from 24 peer-reviewed platelet studies to yield 132 measured kinetic rate constants – that accurately predicts resting levels of cytosolic calcium, IP3, diacylglycerol, phosphatidic acid, phosphoinositol, PIP, and PIP2. The model accurately predicts the full transient calcium dynamics in response to increasing levels of ADP. In the first full stochastic simulation of single platelet response to ADP, the model provides an extremely accurate prediction of the statistics of the asynchronous [Ca]i spikes observed in single platelets. Specifically, this is the first work to provide a quantitative molecular explanation of the asynchronous calcium spiking observed in ADP-activated human platelets. We show the asynchronous spiking is a result of the fundamentally stochastic nature of signal transduction in cells as small as human platelets. Specific testable predictions have emerged about the requirement of high SERCA/IP3R ratios in functional platelets, limits on the concentration of calcium in the DTS, and relative potencies of PAR peptides and ADP. For functional phenotyping platelets, a top-down approach linking multiple inputs to functional outputs was used to understand how human platelets integrate diverse signals encountered during thrombosis. We developed a high-throughput platform that measures the human platelet calcium mobilization in response to all pairwise combinations of six major agonists. Agonists tested in this study were: convulxin (CVX; GPVI activator), ADP, the thromboxane analog U46619, PAR1 agonist peptide (SFLLRN), PAR4 agonist peptide (AYPGKF), and PGE2 (activator of IP and EP receptor). The calcium responses to single agonists at 0.1, 1, 10′ EC50 and 135 pairwise combinations trained a neural network (NN) model to predict the entire 6-dimensional platelet response space. The NN model successfully predicted responses to sequential additions and 27 ternary combinations of [ADP], [convulxin], and [SFLLRN] (R=0.881). With 4077 NN simulations spanning the 6-dimensional agonist space, 45 combinations of 4–6 agonists (ranging from synergism to antagonism) were selected and confirmed experimentally (R=0.883), revealing a highly synergistic condition of high U46619/PGE2 ratio, consistent with the risk of COX-2 therapy. Furthermore, pairwise agonist scanning (PAS) provided a direct measurement of 135 synergy values, thus allowing a unique phenotypic scoring of 10 human donors. Patient-specific training of NNs represent a compact and robust approach for prediction of cellular integration of multiple signals in a complex disease milieu. Either bottom-up models or top-down NN models are ideal for incorporation into systems biology simulations of thrombotic pathways under flow conditions. Disclosures: No relevant conflicts of interest to declare.

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Berndt, Michael C., and Robert K. Andrews. "Systems biology meets platelet biology." Blood 112, no. 10 (November 15, 2008): 3920–21. http://dx.doi.org/10.1182/blood-2008-07-170225.

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Franco, Aime T., Adam Corken, and Jerry Ware. "Platelets at the interface of thrombosis, inflammation, and cancer." Blood 126, no. 5 (July 30, 2015): 582–88. http://dx.doi.org/10.1182/blood-2014-08-531582.

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Abstract Although once primarily recognized for its roles in hemostasis and thrombosis, the platelet has been increasingly recognized as a multipurpose cell. Indeed, circulating platelets have the ability to influence a wide range of seemingly unrelated pathophysiologic events. Here, we highlight some of the notable observations that link platelets to inflammation, reinforcing the platelet’s origin from a lower vertebrate cell type with both hemostatic and immunologic roles. In addition, we consider the relevance of platelets in cancer biology by focusing on the hallmarks of cancer and the ways platelets can influence multistep development of tumors. Beyond its traditional role in hemostasis and thrombosis, the platelet’s involvement in the interplay between hemostasis, thrombosis, inflammation, and cancer is likely complex, yet extremely important in each disease process. The existence of animal models of platelet dysfunction and currently used antiplatelet therapies provide a framework for understanding mechanistic insights into a wide range of pathophysiologic events. Thus, the basic scientist studying platelet function can think beyond the traditional hemostasis and thrombosis paradigms, while the practicing hematologist must appreciate platelet relevance in a wide range of disease processes.

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Masselli, Elena, Giulia Pozzi, Mauro Vaccarezza, Prisco Mirandola, Daniela Galli, Marco Vitale, Cecilia Carubbi, and Giuliana Gobbi. "ROS in Platelet Biology: Functional Aspects and Methodological Insights." International Journal of Molecular Sciences 21, no. 14 (July 9, 2020): 4866. http://dx.doi.org/10.3390/ijms21144866.

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Reactive oxygen species (ROS) and mitochondria play a pivotal role in regulating platelet functions. Platelet activation determines a drastic change in redox balance and in platelet metabolism. Indeed, several signaling pathways have been demonstrated to induce ROS production by NAPDH oxidase (NOX) and mitochondria, upon platelet activation. Platelet-derived ROS, in turn, boost further ROS production and consequent platelet activation, adhesion and recruitment in an auto-amplifying loop. This vicious circle results in a platelet procoagulant phenotype and apoptosis, both accounting for the high thrombotic risk in oxidative stress-related diseases. This review sought to elucidate molecular mechanisms underlying ROS production upon platelet activation and the effects of an altered redox balance on platelet function, focusing on the main advances that have been made in platelet redox biology. Furthermore, given the increasing interest in this field, we also describe the up-to-date methods for detecting platelets, ROS and the platelet bioenergetic profile, which have been proposed as potential disease biomarkers.

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Hundelshausen, Philipp, Frank Petersen, and Ernst Brandt. "Platelet-derived chemokines in vascular biology." Thrombosis and Haemostasis 97, no. 05 (2007): 704–13. http://dx.doi.org/10.1160/th07-01-0066.

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SummaryUndoubtedly, platelets are key elements in the regulation of thrombosis and haemostasis. Along with their primary task to prevent blood loss from injured vessels, platelets have emerged as regulators of a variety of processes in the vasculature. Multiple challenges, from the contact and adhesion to subendothelial matrix after injury of the vessel wall, to interactions with blood cells in inflammatory conditions, result in platelet activation with concomitant shape change and release of numerous substances. Among these, chemokines have been found to modulate several processes in the vasculature, such as atherosclerosis and angiogenesis. In particular, the chemokines connective tissue activating protein III (CTAP-III) and its precursors, or truncation products (CXCL7), platelet factor 4, (PF4, CXCL4) and its variant PF4alt (CXCL4L1) or regulated upon activation and normal T cell expressed and secreted (RANTES, CCL5), have been investigated thoroughly. Defined common properties as their aptitude to bind glycosaminoglycans or their predisposition to associate and form homooligomers are prerequisites for their role in the vasculature and function in vivo. The current review summarizes the development of these single chemokines, and their cooperative effects that may in part be dependent on their physical interactions.

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Littleton-Kearney, Marguerite T., Patricia D. Hurn, Thomas S. Kickler, and Richard J. Traystman. "Incomplete global cerebral ischemia alters platelet biology in neonatal and adult sheep." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 4 (April 1, 1998): H1293—H1300. http://dx.doi.org/10.1152/ajpheart.1998.274.4.h1293.

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Platelets are implicated as etiologic agents in cerebral ischemia and as modulators of neural injury following an ischemic insult. We examined the effects of severe, transient global ischemia on platelet aggregation during 45-min ischemia and 30-, 60-, and 120-min reperfusion in adult and neonatal lambs. We also examined postischemic platelet deposition in brain and other tissues (120-min reperfusion) using indium-111-labeled platelets. Ischemic cerebral blood flow fell to 5 ± 1 and 5 ± 2 ml ⋅ min−1⋅ 100 g−1in lambs and sheep, respectively. During ischemia, platelet counts fell to 47.5 ± 5.1% of control ( P < 0.05) in lambs and 59 ± 4.9% of control in sheep ( P < 0.05). Ischemia depressed platelet aggregation response ( P < 0.01) to 4 μg collagen in lambs and sheep (20.4 ± 29.2 and 26 ± 44.7% of control, respectively). Marked platelet deposition occurred in brain and spleen in sheep, whereas significant platelet entrapment occurred only in brain in lambs. Our findings suggest that ischemia causes platelet activation and deposition in brain and noncerebral tissues.

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Gianazza, Erica, Maura Brioschi, Roberta Baetta, Alice Mallia, Cristina Banfi, and Elena Tremoli. "Platelets in Healthy and Disease States: From Biomarkers Discovery to Drug Targets Identification by Proteomics." International Journal of Molecular Sciences 21, no. 12 (June 25, 2020): 4541. http://dx.doi.org/10.3390/ijms21124541.

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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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Andrade, Sheila Siqueira, Alessandra Valéria de Sousa Faria, Manoel João Batista C. Girão, Gwenny M. Fuhler, Maikel P. Peppelenbosch, and Carmen V. Ferreira-Halder. "Biotech-Educated Platelets: Beyond Tissue Regeneration 2.0." International Journal of Molecular Sciences 21, no. 17 (August 23, 2020): 6061. http://dx.doi.org/10.3390/ijms21176061.

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The increasing discoveries regarding the biology and functions of platelets in the last decade undoubtedly show that these cells are one of the most biotechnological human cells. This review summarizes new advances in platelet biology, functions, and new concepts of biotech-educated platelets that connect advanced biomimetic science to platelet-based additive manufacturing for tissue regeneration. As highly responsive and secretory cells, platelets could be explored to develop solutions that alter injured microenvironments through platelet-based synthetic biomaterials with instructive extracellular cues for morphogenesis in tissue engineering beyond tissue regeneration 2.0.

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De Kock, Lore, and Kathleen Freson. "The (Patho)Biology of SRC Kinase in Platelets and Megakaryocytes." Medicina 56, no. 12 (November 24, 2020): 633. http://dx.doi.org/10.3390/medicina56120633.

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Proto-oncogene tyrosine-protein kinase SRC (SRC), as other members of the SRC family kinases (SFK), plays an important role in regulating signal transduction by different cell surface receptors after changes in the cellular environment. Here, we reviewed the role of SRC in platelets and megakaryocytes (MK). In platelets, inactive closed SRC is coupled to the β subunit of integrin αIIbβ3 while upon fibrinogen binding during platelet activation, αIIbβ3-mediated outside-in signaling is initiated by activation of SRC. Active open SRC now further stimulates many downstream effectors via tyrosine phosphorylation of enzymes, adaptors, and especially cytoskeletal components. Functional platelet studies using SRC knockout mice or broad spectrum SFK inhibitors pointed out that SRC mediates their spreading on fibrinogen. On the other hand, an activating pathological SRC missense variant E527K in humans that causes bleeding inhibits collagen-induced platelet activation while stimulating platelet spreading. The role of SRC in megakaryopoiesis is much less studied. SRC knockout mice have a normal platelet count though studies with SFK inhibitors point out that SRC could interfere with MK polyploidization and proplatelet formation but these inhibitors are not specific. Patients with the SRC E527K variant have thrombocytopenia due to hyperactive SRC that inhibits proplatelet formation after increased spreading of MK on fibrinogen and enhanced formation of podosomes. Studies in humans have contributed significantly to our understanding of SRC signaling in platelets and MK.

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Dissertations / Theses on the topic "Platelet biology"

Hayman, Melissa Anne. "Genomic influences on platelet function." Thesis, Queen Mary, University of London, 2018. http://qmro.qmul.ac.uk/xmlui/handle/123456789/36221.

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The study of platelet messenger and micro-RNAs is of increasing interest owing to the fact that platelets contain the machinery to splice and translate mRNA into proteins in response to inhibitory or activating signals. However, the relatively small size (roughly 4000-5000 transcripts) and short half-life of the platelet transcriptome makes this a technically challenging aspect of platelet biology to investigate. The aims of these thesis investigations were therefore to optimise protocols for the isolation of platelets for downstream RNA analyses and function testing, to investigate the functional capabilities of platelet subpopulations rich in RNA, and to understand the functional and transcriptomic impact of gene mutations predicted to influence platelet function. I found that the optimal method for isolating platelets from whole blood is to use simple single step centrifugation to obtain platelet rich plasma. This method is as effective as more involved methods at reducing white blood cell contamination whilst causing minimal platelet activation. Using this method in combination with flow cytometric cell sorting techniques I was able to isolate the newly formed reticulated platelet sub-population and to confirm the link between reticulation status and increased RNA content. Furthermore, using a range of platelet function assays I demonstrated that reticulated platelets are more reactive than non-reticulated platelets. By obtaining blood samples from a patient with a PLA2G4A mutation I was able to show that loss of cPLA2α enzymatic activity alters both platelet function and the expression of certain mRNA transcripts. My investigations using samples from a range of patients with bleeding tendencies show the benefit of combining deep platelet phenotyping with next generation sequencing to understand the causation of bleeding disorders. Together these investigations highlight the utility of genomic DNA and platelet specific mRNA studies in providing novel insights in to pathways regulating platelet reactivity.

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Wong, Truman. "Dynamics of platelet shape change and aggregation size-dependent platelet subpopulations." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61778.

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Gupta, Nilaksh. "UBIQUITIN-PROTEASOME SYSTEM MODULATES PLATELET FUNCTION." Cleveland State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=csu1408896695.

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Wenger, Roland Hugo. "Platelet molecular biology : cloning and characterisation of the platelet-specific genes CTAP-III and GPIba /." Bern, 1990. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Hill, Sarah Kathleen. "The tetraspanin CD9 localizes to platelet-platelet contacts and regulates thrombus stability." View the abstract Download the full-text PDF version, 2008. http://etd.utmem.edu/ABSTRACTS/2008-036-Hill-index.html.

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Thesis (Ph.D.)--University of Tennessee Health Science Center, 2008.
Title from title page screen (viewed on February 2, 2009). Research advisor: Lisa K. Jennings, Ph.D. Document formatted into pages (xv, 126 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 104-126).

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Gomez, Jorge. "Characterization and regulation of platelet activating factor receptors." Diss., The University of Arizona, 1990. http://hdl.handle.net/10150/185248.

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Platelet activating factor (PAF) is a potent mediator in a variety of inflammatory events. Determining whether PAF participates in the bronchial hyperresponsiveness characteristic of asthma is the long term obj ecti ve for which the studies described here represent an initial step. PAF is a potent agonist that causes contraction of guinea pig peripheral lung strips. To determine if specific receptor sites for PAF could be demonstrated in guinea pig lung membranes (GPLM), direct radioligand binding studies were performed with [³H]C₁₆-PAF (l-0-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine) and the PAF antagonists [³H]WEB 2086 and [³H]RP52770. Binding parameters were compared to those from rabbit platelet membranes (RPM). These studies demonstrated specific binding sites for [³H] C₁₆-PAF of high affinity in GPLM with a Kd of 3 nM,• and in RPM with a K(d) of 1 nM. [³H]C₁₆-PAF identified receptor densities in GPLM of 200 fmol/mg protein and in RPM of 1922 fmol/mg protein. In both tissue preparations binding of inhibited to the same maximum degree by C₁₆-PAF, C₁₈-PAF, WEB 2086, and RP52770, all with pseudo-Hill coefficients of unity. The PAF antagonist [³H]WEB 2086 identified a receptor density similar to that of [³H]C₁₆-PAF. The binding of [³H]WEB 2086 was inhibited to the same degree by C₁₆-PAF, C₁₈-PAF, WEB 2086 and RP52770, indicating WEB 2086 and PAF interact at the same receptor sites in both GPLM and RPM. Although inhibition curves for antagonists yielded pseudo-Hill coefficients of unity, inhibition by agonists yielded shallow inhibition curves suggesting two types or states for the PAF receptor. The PAF antagonist [³H]RP52770 was found to be an unsuitable ligand because it labeled a much larger density of binding sites (1200 fmol/mg protein in GPLM, and 10105 fmol/mg protein in RPM) and was inhibited to little or no extent by C₁₆-PAF, C₁₈-PAF, WEB 2086 or lyso-C₁₆-PAF . studies of signal transduction suggest that the binding affinity of the agonists C₁₆-PAF and C₁₈-PAF (but not for the antagonist WEB 2086) is regulated by GTPgamroa- S and Na⁺, providing indirect evidence that the PAF receptor in both tissue preparations is coupled to a guanine nucleotide regulatory protein. However, agonist binding retained shallow inhibition curves indicating heterogeneity of sites with respect to this regulation. Binding affinity for the agonists was not affected by cholera toxin or pertussis toxin. These results indicate PAF receptors in lung tissue could not be distinguished from those in RPM, however, both tissues appear to show heterogeneity of binding indicating the existence of receptor subtypes or states.

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Bonin, Fanny. "Cytoprotective effects of intracellular platelet activating factor acetylhydrolases." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/26529.

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Platelet activating factor (PAF) is a biologically active phospholipid implicated in the developmental brain disorder Miller-Dieker Syndrome (MDS) and purported to be a primary mediator of cell death in HIV-dementia, ischemia, and epilepsy. As part of my honour's thesis, I demonstrated that PAF can elicit cell death independently of its G-protein coupled receptor (PAFR) in PC12 cells. In my M.Sc. research, I have sought to identify how PAF-mediated cell death is regulated in PC12 cells. PAF is inactivated in brain by two intracellular PAF-acetylhydrolases (PAF-AHs): PAF-AH I and PAF-AH II. PAF-AH I is a trimeric complex composed of two catalytic subunits (alpha1 and alpha2) and one regulatory subunit (beta). Mutations in the Lis1 gene, coding for the beta subunit of PAF-AH I, are the genetic determinant of MDS. However, it is not clear whether these mutations impact on PAF-AH I enzymatic activity in MDS. Furthermore, it is not known whether cytosolic PAF-AH activity regulates the kinetics of neuronal loss following pathophysiological challenge. To begin to address these questions, I sought to identify an in vitro model system suitable for study of PAF-AH activity.* (Abstract shortened by UMI.) *This dissertation is a compound document (contains both a paper copy and a CD as part of the dissertation). The CD requires the following system requirements: QuickTime.

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Kabbani, Nazir. "Chemical-genetic profiling of platelet-activating factor in yeast." Thesis, University of Ottawa (Canada), 2009. http://hdl.handle.net/10393/28189.

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The basic biological processes between the yeast Saccharomyces cerevisiae and mammals are highly conserved. Yeast posses many genes that are implicated in human diseases and have been successfully used as a model for the study of neurodegeneration. Platelet-Activating Factor (C16:0 PAF) causes neuronal cell death independent of its receptor and has been implicated in Alzheimer's disease. I hypothesized that yeast could be used as a model system for deciphering PAF receptor-independent signalling and have utilized genome-wide chemical genomic screening in yeast to further characterize the molecular mechanism of PAF toxicity. Two complementary screens implicate PAF in many cellular processes, some of which parallel results obtained in mammalian studies. I have found that PAF challenge is cytotoxic, delays cell cycle progression, and affects actin stability leading to spindle misorientation and bi-nucleate mother cells.

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Buitrago, Murcia Claudia Lorena. "Cbl proteins in platelet functional responses." Diss., Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/198139.

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Physiology
Ph.D.
c-Cbl protein functions as an E3 ligase and scaffolding protein, where three residues, Y700, Y731, and Y774, upon phosphorylation, have been shown to initiate several signaling cascades. In this study, we investigated the role of these phospho-tyrosine residues in the platelet functional responses upon integrin engagement. We observed that c-Cbl Y700, Y731 and Y774 undergo phosphorylation upon platelet adhesion to immobilized fibrinogen, which was inhibited in the presence of PP2, a pan-src family kinase (SFK) inhibitor, suggesting that c-Cbl is phosphorylated downstream of SFKs. However, OXSI-2, a Syk inhibitor, significantly reduced c-Cbl phosphorylation at residues Y774 and Y700, without affecting Y731 phosphorylation. Interestingly, PP2 inhibited both platelet spreading on fibrinogen as well as clot retraction, whereas OXSI-2 blocked only platelet spreading, suggesting a differential role of these tyrosine residues. The physiological role of c-Cbl and Y731 was studied using platelets from c-Cbl KO and c-CblYF/YF knock-in mice. c-Cbl KO and c-Cbl YF/YF platelets had a significantly reduced spreading over immobilized fibrinogen. Furthermore, clot retraction with c-Cbl KO and c-Cbl YF/YF platelets was drastically delayed. These results indicate that c-Cbl and particularly its phosphorylated residue Y731 plays an important role in platelet outside-in signaling contributing to platelet spreading and clot retraction
Temple University--Theses

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Chase, Peter Burritt 1955. "The molecular pharmacology of a human platelet-activating factor receptor." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/290574.

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Platelet-activating factor (PAF) is a broadly bioactive family of phospholipids which contribute to the pathogenesis of numerous diseases as well as to many normal physiologic processes. The pleiotropic nature of PAFs actions may be due to the activation of several intracellular signaling pathways or the presence of PAF receptor subtypes. Therefore, to begin to understand the complex mechanisms by which PAF molecules induce cellular responses, a molecular approach was initiated to provide tools to investigate many of the issues surrounding PAF receptors. Using a strategy based upon homology cross hybridization, a coding sequence homologous to that of the guinea pig PAF receptor cDNA was identified in a 20 kb insert obtained from human genomic DNA. A portion of the insert was sequenced and appears to be the human homolog of the cloned guinea pig receptor. Although the sequence identity shows that the gene for the human PAF receptor does not contain introns in the coding region, the 5'-untranslated sequence deviates from previously reported cDNA sequences suggesting that at least one intron is present in the untranslated region and represents evidence for alternative mRNA splicing. The 20 kb human genomic fragment also allowed for regional mapping of the PAF receptor gene by fluorescence in situ hybridization and found to localize to chromosome 1 (1p35-> p34.3). Specific localization of the PAF receptor gene to the distal portion of chromosome 1 may assist in understanding the genetic predisposition of certain patients to inflammatory diseases. To examine the second messenger coupling of the cloned PAF receptor and adenylyl cyclase, a cAMP-responsive reporter gene has been used in transiently transfected human choriocarcinoma cells. Preliminary data suggests that PAF receptor signal transduction does result in inhibition of basal and agonist-stimulated adenylyl cyclase activity. PAF receptor specific antibodies could assist in tissue localization of the cloned PAF receptor as well as provide evidence for PAF receptor subtypes. Antibodies were produced against fusion protein consisting of glutathione-S-transferase and a peptide from the purported 2nd extracellular region of the cloned PAF receptor which recognized the native protein in transfected COS-7 cells.

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Books on the topic "Platelet biology"

Schulze, Harald, and Joseph Italiano, eds. Molecular and Cellular Biology of Platelet Formation. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39562-3.

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Rhône-Poulenc Round Table Conference (4th 1985 Menthon-Saint-Bernard, France). Biology and pathology of platelet-vessel wall interactions: Proceedings of the Rhône-Poulenc Santé-INSERM Conference, held at Menthon-Saint-Bernard (Annecy), France, September 30th to October 2nd, 1985. London: Academic Press, 1986.

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Rhône-Poulenc Santé - INSERM Conference (1985 Menthon-Saint-Bernard). Biology and pathology of platelet-vessel wall interactions: Proceedings of the Rhône-Poulenc Santé - INSERM Conference, held at Menthon-Saint-Bernard (Annecy), France, September 30th to October 2nd, 1985. London: Academic Press, 1986.

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International Washington Spring Symposium (11th 1991 George Washington University). Prostaglandins, leukotrienes, lipoxins, and PAF: Mechanism of action, molecular biology, and clinical applications. New York: Plenum Press, 1991.

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1929-, Jamieson G. A., ed. Platelet membrane receptors: Molecular biology, immunology, biochemistry, and pathology : proceedings of the XIXth Annual Scientific Symposium of the American Red Cross held in Washington, DC, October 20-22, 1987. New York: A.R. Liss, 1988.

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Janine, Breton-Gorius, ed. Molecular biology and differentiation of megakaryocytes: Proceedings of the Third International Conference on Megakaryocytes--Megakaryocytes--Cellular and Molecular Biology, held at Conseil Régional de Bourgogne, Dijon, France, July 23-27, 1989. New York: Wiley-Liss, 1990.

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Martin, J. F., and E. A. Trowbridge. Platelet Heterogeneity: Pathology and Biology. Springer-Verlag Berlin and Heidelberg GmbH & Co. KG, 1990.

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Platelet Heterogeneity: Biology and Pathology. Springer, 2012.

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Platelet heterogeneity: Biology and pathology. London: Springer-Verlag, 1990.

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Martin, John. Platelet Heterogeneity: Biology And Pathology. Springer, 2011.

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Book chapters on the topic "Platelet biology"

Thompson, C. B., R. L. Monroy, R. R. Skelly, P. G. Quinn, and J. A. Jakubowski. "The Biology of Platelet Volume Heterogeneity." In Platelet Heterogeneity, 25–37. London: Springer London, 1990. http://dx.doi.org/10.1007/978-1-4471-1763-6_2.

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Mustard, J. F. "Summing Up: Platelet Heterogeneity: Biology and Pathology." In Platelet Heterogeneity, 239–48. London: Springer London, 1990. http://dx.doi.org/10.1007/978-1-4471-1763-6_13.

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Akkerman, Jan-Willem N., and Bernard De Bono. "Systems Biology to Study Platelet-Related Bleeding Disorders." In Platelet Proteomics, 285–320. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470940297.ch12.

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Gardiner, Elizabeth E., Mohammad Al-Tamimi, Robert K. Andrews, and Michael C. Berndt. "Platelet Receptor Shedding." In Methods in Molecular Biology, 321–39. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-307-3_22.

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Flaumenhaft, Robert, and Secil Koseoglu. "Platelet Contents." In Molecular and Cellular Biology of Platelet Formation, 133–52. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39562-3_6.

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Das, P. C., and C. Th Smit Sibinga. "Platelet Freezing." In Cryopreservation and low temperature biology in blood transfusion, 167–78. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1515-5_15.

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Edelstein, Leonard C., and Paul F. Bray. "Noncoding RNAs in Platelet Biology." In Platelets in Thrombotic and Non-Thrombotic Disorders, 239–52. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47462-5_18.

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Shaik, Javed, Ronda Farah, and Maria Hordinsky. "Biology of Platelet-Rich Plasma." In Platelet-Rich Plasma in Dermatologic Practice, 1–12. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-66230-1_1.

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Lopes-Martins, Rodrigo A. B., Claudia V. Araújo, Vanessa Estato, Sheila Moreira, Renato S. B. Cordeiro, and Eduardo V. Tibiriçá. "Platelet-Activating Factor." In Advances in Experimental Medicine and Biology, 223–30. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0179-8_36.

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Gerrard, J. M., L. L. Friesen, J. M. McCrea, S. J. Israels, and P. Robinson. "Platelet Protein Phosphorylation." In Advances in Experimental Medicine and Biology, 235–48. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4615-9442-0_17.

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Conference papers on the topic "Platelet biology"

Sheriff, Jawaad, Phat L. Tran, Marcus Hutchinson, Tracy DeCook, Marvin J. Slepian, Danny Bluestein, and Jolyon Jesty. "The platelet hammer: In vitro platelet activation under repetitive hypershear." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7318350.

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Nachman, R. L., R. L. Silverstein, and A. S. Asch. "THROMBOSPONDIN: CELL BIOLOGY OF AN ADHESIVE GLYCOPROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644653.

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Thrombospondin (TSP), a multifunctional 450 KD glycoprotein is a secretory product of thrombin stimulated platelets. It is a major component of the platelets alpha granule constituting approximately 3% of total platelet protein. Thrombospondin does not circulate in appreciable concentrations ∽0 100 ng/ml); however, the tissue distribution is broad. In addition to its expression on the membrane of activated platelets, the protein is synthesized by fibroblasts endothelial cells, glial cell smooth muscle cells alveolar pneumocytes mononuclear phagocytes and various tumor cells. TSP is a major constituent of the extracellular matrix and has been demonstrated in the vessel wall, basement membrane and glandular connective tissue. Fibroblasts, smooth muscle cells and endothelial cells in tissue culture incorporate TSP into the extracellular matrix. Matrix TSP is under cell-cycle regulatory control. Mesenchymal cells in the proliferative phase synthesize greater amounts of TSP than non growing cells. Platelet derived growth factor induces smooth muscle cell and glial cell synthesis of TSP. Atheromatous lesions contain increased amounts of TSP compared to normal vessels emphasizing the potential role of TSP in the interaction of proliferating cells with the matrix. TSP binds specifically, saturably, and reversibly to mouse peritoneal macrophages and to cells of the monocyte-like human cell line U937. Binding was time dependent and was optimal in the presence of both Ca++ and Mg++. PMA stimulated U937 cells and activated macrophages bound TSP to an equivalent extent as resting cells. The TSP binding site on the surface of U937 cells and peripheral blood monocytes mediates the adhesive interaction between these cells and thrombin-stimulated platelets. Using a sensitive rosetting assay we found that monocytes were not rosetted by resting platelets while >90% were rosetted by thrombin-stimulated platelets. Monoclonal and polyclonal anti-TSP antibodies markedly inhibited rosetting as did TSP itself. Antifibronectin or non-immune control antibodies did not inhibit rosetting, nor did fibronectin, fibrinogen, the fibronectinadhesion tetrapeptide arg-gly-asp-ser (RGDS), or heparin. The TSP membrane receptor, an 88 KD glycoprotein, formely known as GPIV has been identified in platelets, endothelial cells, monocytes and a variety of tumor cells. TSP may thus serve as a molecular bridge linking activated platelets with monocytes at sites of early vascular injury. Such interactions involving the TSP receptor complex may be of critical importance in the regulation of thrombosis and the initiation of atherosclerosis.

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W. Xie, Mingye. "Platelet Application on Wound Healing." In ICCBB '20: 2020 4th International Conference on Computational Biology and Bioinformatics. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3449258.3449267.

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Liang, Xin M., and Nathan J. Sniadecki. "Platelet Nano-Forces are Similar on Fibronectin and Fibrinogen Ligands." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13278.

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We present a new biomechanical approach to measure nanoscale platelet contractile forces, which play an important role in the regulation of hemostasis and thrombosis. Previous studies have indicated that platelets generate contractile forces through actin-myosin interactions that lead to clot retraction and stability. If platelets are unable to generate forces, then the clots they form are loosely-bound and may detach to cause an embolism. Likewise, a higher propensity toward contractility by platelets may cause excessive clot formation in arteries and block blood flow.

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Leung, S. L., A. Dimasi, S. Heiser, A. Dunn, D. Bluestein, and M. Slepian. "Modulation of platelet membrane function via exogenous lipid moiety exposure alters platelet responsiveness to shear." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7318351.

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Bluestein, Danny, João S. Soares, Peng Zhang, Chao Gao, Seetha Pothapragada, Na Zhang, Marvin J. Slepian, and Yuefan Deng. "Multiscale Modeling of Flow Induced Thrombogenicity Using Dissipative Particle Dynamics and Molecular Dynamics." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93094.

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The coagulation cascade of blood may be initiated by flow induced platelet activation, which prompts clot formation in prosthetic cardiovascular devices and arterial disease processes. While platelet activation may be induced by biochemical agonists, shear stresses arising from pathological flow patterns enhance the propensity of platelets to activate and initiate the intrinsic pathway of coagulation, leading to thrombosis. Upon activation platelets undergo complex biochemical and morphological changes: organelles are centralized, membrane glycoproteins undergo conformational changes, and adhesive pseudopods are extended. Activated platelets polymerize fibrinogen into a fibrin network that enmeshes red blood cells. Activated platelets also cross-talk and aggregate to form thrombi. Current numerical simulations to model this complex process mostly treat blood as a continuum and solve the Navier-Stokes equations governing blood flow, coupled with diffusion-convection-reaction equations. It requires various complex constitutive relations or simplifying assumptions, and is limited to μm level scales. However, molecular mechanisms governing platelet shape change upon activation and their effect on rheological properties can be in the nm level scales. To address this challenge, a multiscale approach which departs from continuum approaches, may offer an effective means to bridge the gap between macroscopic flow and cellular scales. Molecular dynamics (MD) and dissipative particle dynamics (DPD) methods have been employed in recent years to simulate complex processes at the molecular scales, and various viscous fluids at low-to-high Reynolds numbers at mesoscopic scales. Such particle methods possess important properties at the mesoscopic scale: complex fluids with heterogeneous particles can be modeled, allowing the simulation of processes which are otherwise very difficult to solve by continuum approaches. It is becoming a powerful tool for simulating complex blood flow, red blood cells interactions, and platelet-mediated thrombosis involving platelet activation, aggregation, and adhesion.

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Yagi, Asuka, Yoshihiro Kuroda, Yuki Uranishi, Masataka Imura, and Osamu Oshiro. "3D simulation of platelet aggregation in cryosurgery." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6609894.

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Smagin, M. A., A. Iu Demura, O. A. Shumkov, M. Iu Soluyanov, O. V. Poveshenko, and V. V. Nimaev. "Platelet-rich plasma in treatment of non-healing ulcers." In 2018 11th International Multiconference Bioinformatics of Genome Regulation and Structure\Systems Biology (BGRS\SB). IEEE, 2018. http://dx.doi.org/10.1109/csgb.2018.8544810.

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Valerio, Lorenzo, Filippo Consolo, Danny Bluestein, Phat Tran, Marvin Slepian, Alberto Redaelli, and Federico Pappalardo. "Shear-mediated platelet activation in patients implanted with continuous flow LVADs: A preliminary study utilizing the platelet activity state (PAS) assay." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7318595.

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Sadler, J. Evan. "THE MOLECULAR BIOLOGY OF VON WILLEBRAND FACTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643930.

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Human von Willebrand factor (vWF) is a plasma glycoprotein that is synthesized by endothelial cells and megakaryocytes, and perhaps by syncytiotrophoblast of placenta. The biosynthesis of vWF is very complex, involving proteolytic processing, glycosyla-tion, disulfide bond formation, and sulfation. Mature vWF consists of a single subunit of ∼ 250,000 daltons that is assembled into multimer ranging from dimers to species of over 10 million daltons. vWF performs its essential hemostatic function through several binding interactions, forming a bridge between specific receptors on the platelet surface and components of damaged vascular subendothelial connective tissue. Inherited deficiency of vWF, or von Willebrand disease (vWD), is the most common genetically transmitted bleeding disorder worldwide. The last two years has been a time of very rapid progress in understanding the molecular biology of vWF. Four research groups have independently isolated and sequenced the 9 kilobase full-length vWF cDNA. The predicted protein sequence has provided a foundation for understanding the biosynthetic processing of vWF, and has clarified the relationship between vWF and a 75-100 kilodalton plasma protein of unknown function, von Willebrand antigen II (vWAgll)/ vWAgll is co-distributed with vWF in endothelial cells and platelets, and is deficient in patients with vWD. The cDNA sequence of vWF shows that vWAgll is a rather large pro-peptide for vWF, explaining the biochemical and genetic association between the two proteins. vWF has a complex evolutionary history marked by many separate gene segment duplications. The primary structure of the protein contains four distinct types of repeated domains present in two to four copies each. Repeated domains account for over 90 percent of the protein sequence. This sequence provides a framework for ordering the functional domains that have been defined by protein chemistry methods. A tryptic peptide from the amino-terminus of vWF that overlaps domain D3 binds to factor VIII and also appears to bind to heparin. Peptides that include domain A1 bind to collagens, to heparin, and to platelet glycoprotein Ib. A second collagen binding site appears to lie within domain A3. The vWF cDNA has been expressed in heterologous cells to produce small amounts of functionally and structurally normal vWF, indicating that endothelial cells are not unique in their ability to process and assemble vWF multimers. Site-directed mutagenesis has been used to show that deletion of the propeptide of vWF prevents the formation of multimers. Cloned cDNA probes have been employed to isolate vWF genomic DNA from cosmid and λ-phage libraries, and the size of the vWF gene appears to be ∼ 150 kilobases. The vWF locus has been localized to human chromosome 12p12—pter. Several intragenic RFLPs have been characterized. With them, vWF has been placed on the human genetic linkage map as the most telomeric marker currently available for the short arm of chromosome 12. A second apparently homologous locus has been identified on chromosome 22, but the relationship of this locus to the authentic vWF gene is not yet known. The mechanism of vWD has been studied by Southern blotting of genomic DNA with cDNA probes in a few patients. Three unrelated pedigrees have been shown to have total deletions of the vWF gene as the cause of severe vWD (type III). This form of gene deletion appears to predispose to the development of inhibitory alloantibodies to vWF during therapy with cryoprecipitate. During the next several years recombinant DNA methods will continue to contribute our understanding of the evolution, biosynthesis, and structure-function relationships of vWF, as well as the mechanism of additional variants of vWD at the level of gene structure.

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