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1. Modeling Platelet P2Y$_1$/$_{12}$ Pathway to Integrin Activation

Author

Patel, Keshav B., Bergmeier, Wolfgang, and Fogelson, Aaron L.

Subjects
Quantitative Biology - Molecular Networks, Quantitative Biology - Subcellular Processes
Abstract

Through experimental studies, many details of the pathway of integrin $\alpha_{\rm IIb}\beta_3$ activation by ADP during the platelet aggregation process have been mapped out. ADP binds to two separate G protein coupled receptors on platelet surfaces, leading to alterations in the regulation of the small GTPase RAP1. We seek to (1) gain insights into the relative contributions of both pathways to RAP1-mediated integrin activation and to (2) predict cell behavior in response to a continuous range of external agonist concentrations. To this end, we develop a dynamical systems model detailing the action of each protein in the two pathways up to the regulation of RAP1. We perform a parameter estimation using flow cytometry data to determine a number of unknown rate constants. We then validate with already published data; in particular, the model confirmed the effect of impaired P2Y$_1$ receptor desensitization or reduced RASA3 expression on RAP1 activation. We then predict the effect of protein expression levels on integrin activation and show that components of the P2Y$_{12}$ pathway are critical to the regulation of integrin. This model aids in our understanding of interindividual variability in platelet response to ADP and therapeutic P2Y$_{12}$ inhibition. It also provides a more detailed view of platelet activation in the ongoing mathematical study of platelet aggregation.

Published
2024

15. Advances in Clinical and Basic Science of Coagulation: Illustrated abstracts of the 9th Chapel Hill Symposium on Hemostasis

Author

Bergmeier, Wolfgang, Antoniak, Silvio, Conway, Edward M, Denis, Cécile V, George, Lindsey A, Isermann, Berend, Key, Nigel S, Krishnaswamy, Sriram, Lam, Wilbur A, Lillicrap, David, Liu, Jian, Looney, Mark R, López, José A, Maas, Coen, Peyvandi, Flora, Ruf, Wolfram, Sood, Anil K, Versteeg, Henri H, Wolberg, Alisa S, Wong, Pancras C, Wood, Jeremy P, and Weiler, Hartmut

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

This 9th Symposium on Hemostasis is an international scientific meeting held biannually in Chapel Hill, North Carolina. The meeting is in large measure the result of the close friendship between the late Dr. Harold R. Roberts of UNC Chapel Hill and Dr. Ulla Hedner of Novo Nordisk. When Novo Nordisk was developing the hemophilia therapy that would become NovoSeven, they sponsored a series of meetings to understand the basic biology and clinical applications of factor VIIa. The first meeting in Chapel Hill was held April 4-6, 2002 with Dr. Roberts as the organizer. Over the years, the conference emphasis has expanded from discussions of factor VIIa and tissue factor to additional topics in hemostasis and thrombosis. This year's meeting includes presentations by internationally renowned speakers that discuss the state-of-the-art on an array of important topics, including von Willebrand factor, engineering advances, coagulation and disease, tissue factor biology, therapeutic advances, and basic clotting factor biology. Included in this review article are illustrated abstracts provided by our speakers, which highlight the main conclusions of each invited talk. This will be the first meeting without Dr. Roberts in attendance, yet his commitment to excellent science and his focus on turning science to patient care are pervasively reflected in the presentations by our speakers.

Published
2018

17. Utility of thromboelastography with platelet mapping for monitoring platelet transfusion in qualitative platelet disorders

Author

Lee, Robert H., Rudran, Tanvi, and Bergmeier, Wolfgang

Abstract

Patients with pathogenic variants in RASGRP2(inherited platelet disorder (IPD)-18) exhibit normal platelet counts but impaired platelet aggregation and αIIbβ3activation. Moderate-to-severe bleeding episodes require patients to be transfused with platelets and/or pro-hemostatic agents. We recently demonstrated that hemostatic efficacy of transfused platelets is limited by dysfunctional endogenous platelets in a mouse model of IPD-18 (Rasgrp2−/−mice), as dysfunctional platelets were recruited to the forming hemostatic plug but did not participate in clot contraction. Thus, higher amounts of transfused platelets were required to outcompete these dysfunctional cells and to reverse bleeding.

Published
2024
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18. Specifications of the variant curation guidelines for ITGA2B/ITGB3: ClinGen Platelet Disorder Variant Curation Panel

Author

Ross, Justyne E., Zhang, Bing M., Lee, Kristy, Mohan, Shruthi, Branchford, Brian R., Bray, Paul, Dugan, Stefanie N., Freson, Kathleen, Heller, Paula G., Kahr, Walter H.A., Lambert, Michele P., Luchtman-Jones, Lori, Luo, Minjie, Perez Botero, Juliana, Rondina, Matthew T., Ryan, Gabriella, Westbury, Sarah, Bergmeier, Wolfgang, and Di Paola, Jorge

Published
2021
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19. Megakaryocytes use in vivo podosome‐like structures working collectively to penetrate the endothelial barrier of bone marrow sinusoids

Author

Eckly, Anita, Scandola, Cyril, Oprescu, Antoine, Michel, Deborah, Rinckel, Jean‐Yves, Proamer, Fabienne, Hoffmann, David, Receveur, Nicolas, Léon, Catherine, Bear, James E., Ghalloussi, Dorsaf, Harousseau, Gabriel, Bergmeier, Wolfgang, Lanza, Francois, Gaits‐Iacovoni, Frédérique, de la Salle, Henri, and Gachet, Christian

Published
2020
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20. Illustrated State‐of‐the‐Art Capsules of the ISTH 2020 Congress

Author

Ariens, Robert, Becattini, Cecilia, Bender, Markus, Bergmeier, Wolfgang, Castoldi, Elisabetta, Devreese, Katrien, Ellis, Martin, Gailani, David, Ignjatovic, Vera, James, Paula D., Kerrigan, Steven, Lambert, Michele, Lee, Lai Heng, Levi, Marcel, Maugeri, Norma, Meijers, Joost, Melero‐Martin, Juan, Michelson, Alan D., Mingozzi, Federico, Neeves, Keith, Ni, Heyu, Olsson, Anna‐Karin, Prohászka, Zoltán, Ranson, Marie, Riva, Nicoletta, Senis, Yotis, van Ommen, Cornelia H., Vaughan, Douglas E., and Weisel, John

Published
2020
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26. Mice expressing nonpolymerizable fibrinogen have reduced arterial and venous thrombosis with preserved hemostasis

Author

Hur, Woosuk Steve, primary, Kawano, Tomohiro, additional, Mwiza, Jean Marie N., additional, Paul, David S., additional, Lee, Robert H., additional, Clark, Emily G, additional, Bouck, Emma G, additional, Dutta, Ananya, additional, Cai, Can, additional, Baker, Stephen R, additional, Guthold, Martin, additional, Mackman, Nigel, additional, Mangin, Pierre H., additional, Wolberg, Alisa S., additional, Bergmeier, Wolfgang, additional, and Flick, Matthew J., additional

Published
2023
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27. GTPases

Author

Stefanini, Lucia, Lee, Robert H., Bergmeier, Wolfgang, Gresele, Paolo, editor, Kleiman, Neal S., editor, Lopez, José A., editor, and Page, Clive P., editor

Published
2017
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29. Regulation of Platelet Granule Exocytosis by S-Nitrosylation

Author

Morrell, Craig N., Matsushita, Kenji, Chiles, Kelly, Scharpf, Robert B., Yamakuchi, Munekazu, Bergmeier, Wolfgang, Mankowski, Joseph L., Baldwin,, William M., Faraday, Nauder, Lowenstein, Charles J., and Ignarro, Louis J.

Published
2005

32. Platelet biology and function: plaque erosion vs. rupture.

Author

Baaten, Constance C F M J, Nagy, Magdolna, Bergmeier, Wolfgang, Spronk, Henri M H, and Meijden, Paola E J van der

Subjects
BLOOD platelet activation, BIOLOGY, ATHEROSCLEROTIC plaque, FIBRINOLYTIC agents, BLOOD platelets
Abstract

The leading cause of heart disease in developed countries is coronary atherosclerosis, which is not simply a result of ageing but a chronic inflammatory process that can lead to acute clinical events upon atherosclerotic plaque rupture or erosion and arterial thrombus formation. The composition and location of atherosclerotic plaques determine the phenotype of the lesion and whether it is more likely to rupture or to erode. Although plaque rupture and erosion both initiate platelet activation on the exposed vascular surface, the contribution of platelets to thrombus formation differs between the two phenotypes. In this review, plaque phenotype is discussed in relation to thrombus composition, and an overview of important mediators (haemodynamics, matrix components, and soluble factors) in plaque-induced platelet activation is given. As thrombus formation on disrupted plaques does not necessarily result in complete vessel occlusion, plaque healing can occur. Therefore, the latest findings on plaque healing and the potential role of platelets in this process are summarized. Finally, the clinical need for more effective antithrombotic agents is highlighted. [ABSTRACT FROM AUTHOR]

Published
2024
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33. The CalDAG-GEFI/Rap1/aIIbß3 axis minimally contributes to accelerated platelet clearance in mice with constitutive store-operated calcium entry.

Author

Lee, Robert H., Rocco, David J., Nieswandt, Bernhard, and Bergmeier, Wolfgang

Subjects
BLOOD platelets, PLATELET count, MICE, CALCIUM, ESOPHAGEAL varices, BLOOD platelet disorders, INTEGRINS
Abstract

Circulating platelets maintain low cytosolic Ca2+ concentrations. At sites of vascular injury, agonist-induced Ca2+ release from platelet intracellular stores triggers influx of extracellular Ca2+, a process known as store-operated Ca2+ entry (SOCE). Stromal interaction molecule 1 (Stim1) senses reduced Ca2+ stores and triggers SOCE. Gain-of-function (GOF) mutations in Stim1, such as described for Stormorken syndrome patients or mutant mice (Stim1Sax), are associated with marked thrombocytopenia and increased platelet turnover. We hypothesized that reduced platelet survival in Stim1Sax/+ mice is due to increased Rap1/integrin signaling and platelet clearance in the spleen, similar to what we recently described for mice expressing a mutant version of the Rap1-GAP, Rasa3 (Rasa3hlb/hlb). Stim1Sax/+ mice were crossed with mice deficient in CalDAG-GEFI, a critical calcium-regulated Rap1-GEF in platelets. In contrast to Rasa3hlb/hlb x Caldaggef1-/- mice, only a small increase in the peripheral platelet count, but not platelet lifespan, was observed in Stim1Sax/+ x Caldaggef1-/- mice. Similarly, inhibition of aIIbß3 integrin in vivo only minimally raised the peripheral platelet count in Stim1Sax/+ mice. Compared to controls, Stim1Sax/+ mice exhibited increased platelet accumulation in the lung, but not the spleen or liver. These results suggest that CalDAG-GEFI/Rap1/integrin signaling contributes only minimally to accelerated platelet turnover caused by constitutive SOCE. [ABSTRACT FROM AUTHOR]

Published
2023
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34. Contributors

Author

Alsousou, Joseph, primary, Angiolillo, Dominick J., additional, Arachiche, Amal, additional, Aster, Richard H., additional, Barbui, Tiziano, additional, Basili, Stefania, additional, Battinelli, Elisabeth M., additional, Bavry, Anthony A., additional, Bergmeier, Wolfgang, additional, Bertrand, Gerald, additional, Bhatt, Deepak L., additional, Blair, Thomas A., additional, Bledzka, Kamila, additional, Borst, Oliver, additional, Bouck, Emma G., additional, Brass, Lawrence F., additional, Bray, Paul F., additional, Briggs, Carol, additional, Brzoska, Tomasz, additional, Bussel, James B., additional, Cattaneo, Marco, additional, Chakravorty, Subarna, additional, Chan, Noel C., additional, Chaturvedi, Shruti, additional, Chong, Beng H., additional, Clemetson, Kenneth J., additional, Clemetson, Jeannine M., additional, Coller, Barry S., additional, del Zoppo, Gregory J., additional, Despotovic, Jenny M., additional, Diamond, Scott L., additional, Easton, J. Donald, additional, Eto, Koji, additional, Falet, Hervé, additional, Ferrer-Marin, Francisca, additional, Finazzi, Guido, additional, Flaumenhaft, Robert, additional, Freedman, Jane E., additional, Frelinger, Andrew L., additional, Freson, Kathleen, additional, Gasecka, Aleksandra, additional, Gawaz, Meinrad, additional, Giannini, Silvia, additional, Greinacher, Andreas, additional, Gremmel, Thomas, additional, Gurbel, Paul A., additional, Haining, Elizabeth J., additional, Han, Xu, additional, Harrison, Paul, additional, Hayward, Catherine P.M., additional, Hoffmeister, Karin, additional, Hvas, Anne-Mette, additional, Israels, Sara J., additional, Italiano, Joseph E., additional, Jeong, Young-Hoon, additional, Johnson, Andrew D., additional, Kaplan, Cecile, additional, Karagiannis, Peter, additional, Kato, Gregory J., additional, Kemble, Samuel, additional, Kolandaivelu, Kumaran, additional, Koupenova, Milka, additional, Kuter, David J., additional, Lambert, Michele P., additional, Lee, Robert H., additional, Levin, Jack, additional, Li, Renhao, additional, Li, Zhenyu, additional, Li, Zihai, additional, Li, Anqi, additional, Liani, Rossella, additional, Lordkipanidzé, Marie, additional, Lorenz, Viola, additional, Machlus, Kellie R., additional, Mahtta, Dhruv, additional, Mannucci, Pier Mannuccio, additional, McCrae, Keith R., additional, Metelli, Alessandra, additional, Michelson, Alan D., additional, Moffat, Karen A., additional, Moon, Jae Youn, additional, Morrissey, James H., additional, Mutch, Nicola J., additional, Nagy, Zoltan, additional, Ni, Heyu, additional, Nicolson, Phillip L.R., additional, Nieman, Marvin T., additional, Nieuwland, Rienk, additional, Onselaer, Marie-Blanche, additional, Patrono, Carlo, additional, Plow, Edward F., additional, Poncz, Mortimer, additional, Poon, Man-Chiu, additional, Poulter, Natalie S., additional, Poventud-Fuentes, Izmarie, additional, Provost, Patrick, additional, Qin, Jun, additional, Rayes, Julie, additional, Reiner, Alexander P., additional, Riesenberg, Brian, additional, Roberts, Irene A.G., additional, Rondina, Matthew T., additional, Rowley, Jesse W., additional, Santilli, Francesca, additional, Scharf, Rüdiger E., additional, Senis, Yotis A., additional, Sharda, Anish, additional, Siddon, Alexa J., additional, Siljander, Pia R.-M., additional, Tricoci, Pierluigi, additional, Simeone, Paola, additional, Smith, Stephanie A., additional, Smyth, Susan S., additional, Snyder, Edward L., additional, Sola-Visner, Martha, additional, Stalker, Timothy J., additional, Stefanini, Lucia, additional, Sugimoto, Naoshi, additional, Sundd, Prithu, additional, Tantry, Udaya S., additional, Tefferi, Ayalew, additional, Thomas, Steven G., additional, Thomas, Mark R., additional, Tomaiuolo, Maurizio, additional, Tormey, Christopher A., additional, Tsai, Han-Mou, additional, Violi, Francesco, additional, Warkentin, Theodore E., additional, Watson, Steve P., additional, Weitz, Jeffrey I., additional, Welsh, John, additional, Weyrich, Andrew S., additional, Wilcox, David A., additional, Wu, Bill X., additional, Yeaman, Michael R., additional, Zhu, Li, additional, Zimmerman, Guy A., additional, and Zunica, Elizabeth R., additional

Published
2019
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38. Abstract 143: Differential Suppression Of Arterial Versus Venous Thrombosis But Preserved Hemostasis In Mice Expressing Fibrinogen That Cannot Support Fibrin Formation

Author

Hur, Woosuk S, primary, Kawano, Tomohiro, additional, Mwiza, Jean M, additional, Paul, David, additional, Lee, Robert, additional, Clark, Emily, additional, Bouck, Emma, additional, Mackman, Nigel, additional, Wolberg, Alisa S, additional, Bergmeier, Wolfgang, additional, and Flick, Matthew J, additional

Published
2023
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40. Novel mutations in RASGRP2, which encodes CalDAG-GEFI, abrogate Rap1 activation, causing platelet dysfunction

Author

Lozano, María Luisa, Cook, Aaron, Bastida, José María, Paul, David S., Iruin, Gemma, Cid, Ana Rosa, Adan-Pedroso, Rosa, Ramón González-Porras, José, Hernández-Rivas, Jesús María, Fletcher, Sarah J., Johnson, Ben, Morgan, Neil, Ferrer-Marin, Francisca, Vicente, Vicente, Sondek, John, Watson, Steve P., Bergmeier, Wolfgang, and Rivera, José

Published
2016
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44. Sugar makes neutrophils RAGE: linking diabetes-associated hyperglycemia to thrombocytosis and platelet reactivity

Author

Lee, Robert H. and Bergmeier, Wolfgang

Subjects
Thrombocytosis -- Physiological aspects, Hyperglycemia -- Physiological aspects, Neutrophils -- Health aspects, Health care industry
Abstract

Diabetes mellltus Is associated with an Increased risk for cardiovascular disease, but the link between hyperglycemia and atherothrombotic disease is not completely understood. Patients with diabetes often show hyporesponsiveness to antiplatelet therapies, and it has been suggested that hyperreactive reticulated platelets underlie this altered therapeutic response. In this issue of the JCI, Kraakman et al. uncover a previously unknown link between hyperglycemia and enhanced platelet production and reactivity. The authors demonstrate that high blood glucose levels trigger neutrophil release of S100 calcium-binding protein A8/A9 (S100A8/ A9), which binds to the receptor for advanced glycation end products (RAGE) on Kupffer cells, ultimately leading to increased thrombopoietin (TPO) production in the liver. TPO causes megakaryocyte proliferation and increased platelet production. This study demonstrates the importance of glycemic control and identifies potential therapeutic targets in the normalization of platelet numbers and function in diabetes., Introduction Diabetes mellitus is a disease characterized by an inability of the body to produce or respond to insulin, resulting in hyperglycemia. Type 1 diabetes (T1D) is caused by autoimmune [...]

Published
2017
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