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730 results on '"Bergmeier, Wolfgang"'

202. Regulated surface expression and shedding support a dual role for semaphorin 4D in platelet responses to vascular injury

Author

Zhu, Li, primary, Bergmeier, Wolfgang, additional, Wu, Jie, additional, Jiang, Hong, additional, Stalker, Timothy J., additional, Cieslak, Marcin, additional, Fan, Ran, additional, Boumsell, Laurence, additional, Kumanogoh, Atsushi, additional, Kikutani, Hitoshi, additional, Tamagnone, Luca, additional, Wagner, Denisa D., additional, Milla, Marcos E., additional, and Brass, Lawrence F., additional

Published
2007
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209. Systemic antithrombotic effects of ADAMTS13

Author

Chauhan, Anil K., primary, Motto, David G., additional, Lamb, Colin B., additional, Bergmeier, Wolfgang, additional, Dockal, Michael, additional, Plaimauer, Barbara, additional, Scheiflinger, Friedrich, additional, Ginsburg, David, additional, and Wagner, Denisa D., additional

Published
2006
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211. Erratum: CalDAG-GEFI integrates signaling for platelet aggregation and thrombus formation

Author

Crittenden, Jill R, Bergmeier, Wolfgang, Zhang, Yanyu, Piffath, Crystal L, Liang, Yuqiong, Wagner, Denisa D, Housman, David E, and Graybiel, Ann M

Abstract

Author(s): Jill R Crittenden; Wolfgang Bergmeier; Yanyu Zhang; Crystal L Piffath; Yuqiong Liang; Denisa D Wagner; David E Housman; Ann M Graybiel Nat. Med. 10, 982-986 (2004) Supplementary Video 2 [...]

Published
2004
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217. Regulation of platelet granule exocytosis by S-nitrosylation

Author

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

Published
2005
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225. Antithrombotic activity of TNF-α

Author

Cambien, Beatrice, primary, Bergmeier, Wolfgang, additional, Saffaripour, Simin, additional, Mitchell, Heather A., additional, and Wagner, Denisa D., additional

Published
2003
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226. Mechanisms and implications of platelet discoid shape

Author

Italiano, Joseph E., primary, Bergmeier, Wolfgang, additional, Tiwari, Sanjay, additional, Falet, Hervé, additional, Hartwig, John H., additional, Hoffmeister, Karin M., additional, André, Patrick, additional, Wagner, Denisa D., additional, and Shivdasani, Ramesh A., additional

Published
2003
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229. Mice expressing nonpolymerizable fibrinogen have reduced arterial and venous thrombosis with preserved hemostasis

Author

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

Abstract

•Mice expressing nonpolymerizable fibrinogen are protected against venous thrombosis and have suppressed arterial thrombosis.•Selective prevention of fibrin polymerization had minimal influence on hemostasis.

Published
2023
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230. Distinct bidirectional regulation of LFA1 and α4β7 by Rap1 and integrin adaptors in T cells under shear flow

Author

Kamioka, Yuji, Ueda, Yoshihiro, Kondo, Naoyuki, Tokuhiro, Keizo, Ikeda, Yoshiki, Bergmeier, Wolfgang, and Kinashi, Tatsuo

Abstract

Bidirectional control of integrin activation plays crucial roles in cell adhesive behaviors, but how integrins are specifically regulated by inside-out and outside-in signaling has not been fully understood. Here, we report distinct bidirectional regulation of major lymphocyte homing receptors LFA1 and α4β7 in primary T cells. A small increase of Rap1 activation in L-selectin-mediated tether/rolling was boosted by the outside-in signaling from ICAM1-interacting LFA1 through subsecond, simultaneous activation of Rap1 GTPase and talin1, but not kindlin-3, resulting in increased capture and slowing. In contrast, none of them were required for tether/rolling by α4β7 on MAdCAM1. High Rap1 activation with chemokines or the loss of Rap1-inactivating proteins Rasa3 and Sipa1 increased talin1/kindlin-3-dependent arrest with high-affinity binding of LFA1 to membrane-anchored ICAM1. However, despite increased affinity of α4β7, activated Rap1 severely suppressed adhesion on MAdCAM1 under shear flow, indicating the critical importance of a sequential outside-in/inside-out signaling for α4β7.

Published
2023
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231. Protease-activated receptors and glycoprotein VI cooperatively drive the platelet component in thromboelastography

Author

Rudran, Tanvi, Antoniak, Silvio, Flick, Matthew J., Ginsberg, Mark H., Wolberg, Alisa S., Bergmeier, Wolfgang, and Lee, Robert H.

Abstract

Thromboelastography (TEG) is used for real-time determination of hemostatic status in patients with acute risk of bleeding. Thrombin is thought to drive clotting in TEG through generation of polymerized fibrin and activation of platelets through protease-activated receptors (PARs). However, the specific role of platelet agonist receptors and signaling in TEG has not been reported.

Published
2023
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232. Loss of P2Y1receptor desensitization does not impact hemostasis or thrombosis despite increased platelet reactivity in vitro

Author

Paul, David S., Blatt, Tasha N., Schug, Wyatt J., Clark, Emily G., Kawano, Tomohiro, Mackman, Nigel, Murcia, Sebastian, Poe, Kathryn O., Mwiza, Jean Marie N., Harden, T. Kendall, Bergmeier, Wolfgang, and Nicholas, Robert A.

Abstract

Hemostatic plug formation at sites of vascular injury is strongly dependent on rapid platelet activation and integrin-mediated adhesion and aggregation. However, to prevent thrombotic complications, platelet aggregate formation must be a self-limiting process. The second wave mediator ADP activates platelets via Gq-coupled P2Y1and Gi-coupled P2Y12receptors. Following ADP exposure, the P2Y1receptor undergoes rapid phosphorylation-induced desensitization, a negative feedback mechanism thought to be critical for limiting thrombus growth.

Published
2023
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235. Flow-Cytometric Analysis of Mouse Platelet Function.

Author

Walker, John M., Gibbins, Jonathan M., Mahaut-Smith, Martyn P., Nieswandt, Bernhard, Schulte, Valerie, and Bergmeier, Wolfgang

Abstract

Characterization of platelet-membrane glycoproteins and their intracellular signaling pathways has become essential to understanding platelet function not only in the context of thrombosis and hemostasis, but also other processes like inflammation, tumor metastasis, and atherosclerosis. Besides their central role in these processes in vivo, platelets are increasingly used as a convenient and physiologically relevant model for basic studies on cell adhesion and signaling processes. [ABSTRACT FROM AUTHOR]

Published
2004
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239. 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

Abstract

In addition to mutations in ITG2B or ITGB3 genes that cause defective αIIbβ3 expression and/or function in Glanzmann’s thrombasthenia patients, platelet dysfunction can be a result of genetic variability in proteins that mediate inside-out activation of αIIbβ3. The RASGRP2 gene is strongly expressed in platelets and neutrophils, where its encoded protein CalDAG-GEFI facilitates the activation of Rap1 and subsequent activation of integrins. We used next-generation sequencing (NGS) and whole-exome sequencing (WES) to identify 2 novel function-disrupting mutations in RASGRP2 that account for bleeding diathesis and platelet dysfunction in 2 unrelated families. By using a panel of 71 genes, we identified a homozygous change (c.1142C>T) in exon 10 of RASGRP2 in a 9-year-old child of Chinese origin (family 1). This variant led to a p.Ser381Phe substitution in the CDC25 catalytic domain of CalDAG-GEFI. In 2 Spanish siblings from family 2, WES identified a nonsense homozygous variation (c.337C>T) (p.Arg113X) in exon 5 of RASGRP2. CalDAG-GEFI expression was markedly reduced in platelets from all patients, and by using a novel in vitro assay, we found that the nucleotide exchange activity was dramatically reduced in CalDAG-GEFI p.Ser381Phe. Platelets from homozygous patients exhibited agonist-specific defects in αIIbβ3 integrin activation and aggregation. In contrast, α- and δ-granule secretion, platelet spreading, and clot retraction were not markedly affected. Integrin activation in the patients’ neutrophils was also impaired. These patients are the first cases of a CalDAG-GEFI deficiency due to homozygous RASGRP2 mutations that are linked to defects in both leukocyte and platelet integrin activation.

Published
2016
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240. Synthesis and dephosphorylation of MARCKS in the late stages of megakaryocyte maturation drive proplatelet formation

Author

Machlus, Kellie R., Wu, Stephen K., Stumpo, Deborah J., Soussou, Thomas S., Paul, David S., Campbell, Robert A., Kalwa, Hermann, Michel, Thomas, Bergmeier, Wolfgang, Weyrich, Andrew S., Blackshear, Perry J., Hartwig, John H., and Italiano, Joseph E.

Abstract

Platelets are essential for hemostasis, and thrombocytopenia is a major clinical problem. Megakaryocytes (MKs) generate platelets by extending long processes, proplatelets, into sinusoidal blood vessels. However, very little is known about what regulates proplatelet formation. To uncover which proteins were dynamically changing during this process, we compared the proteome and transcriptome of round vs proplatelet-producing MKs by 2D difference gel electrophoresis (DIGE) and polysome profiling, respectively. Our data revealed a significant increase in a poorly-characterized MK protein, myristoylated alanine-rich C-kinase substrate (MARCKS), which was upregulated 3.4- and 5.7-fold in proplatelet-producing MKs in 2D DIGE and polysome profiling analyses, respectively. MARCKS is a protein kinase C (PKC) substrate that binds PIP2. In MKs, it localized to both the plasma and demarcation membranes. MARCKS inhibition by peptide significantly decreased proplatelet formation 53%. To examine the role of MARCKS in the PKC pathway, we treated MKs with polymethacrylate (PMA), which markedly increased MARCKS phosphorylation while significantly inhibiting proplatelet formation 84%, suggesting that MARCKS phosphorylation reduces proplatelet formation. We hypothesized that MARCKS phosphorylation promotes Arp2/3 phosphorylation, which subsequently downregulates proplatelet formation; both MARCKS and Arp2 were dephosphorylated in MKs making proplatelets, and Arp2 inhibition enhanced proplatelet formation. Finally, we used MARCKS knockout (KO) mice to probe the direct role of MARCKS in proplatelet formation; MARCKS KO MKs displayed significantly decreased proplatelet levels. MARCKS expression and signaling in primary MKs is a novel finding. We propose that MARCKS acts as a “molecular switch,” binding to and regulating PIP2signaling to regulate processes like proplatelet extension (microtubule-driven) vs proplatelet branching (Arp2/3 and actin polymerization-driven).

Published
2016
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241. Rap1 and its effector RIAM are required for lymphocyte trafficking

Author

Su, Wenjuan, Wynne, Joseph, Pinheiro, Elaine M., Strazza, Marianne, Mor, Adam, Montenont, Emilie, Berger, Jeffrey, Paul, David S., Bergmeier, Wolfgang, Gertler, Frank B., and Philips, Mark R.

Abstract

Regulation of integrins is critical for lymphocyte adhesion to endothelium and trafficking through secondary lymphoid organs. Inside-out signaling to integrins is mediated by the small GTPase Rap1. Two effectors of Rap1 regulate integrins, RapL and Rap1 interacting adaptor molecule (RIAM). Using mice conditionally deficient in both Rap1a and Rap1b and mice null for RIAM, we show that the Rap1/RIAM module is not required for T- or B-cell development but is essential for efficient adhesion to intercellular adhesion molecule (ICAM) 1 and vascular cell adhesion molecule (VCAM) 1 and for proper trafficking of lymphocytes to secondary lymphoid organs. Interestingly, in RIAM-deficient mice, whereas peripheral lymph nodes (pLNs) were depleted of both B and T cells and recirculating B cells were diminished in the bone barrow (BM), the spleen was hypercellular, albeit with a relative deficiency of marginal zone B cells. The abnormality in lymphocyte trafficking was accompanied by defective humoral immunity to T-cell–dependent antigens. Platelet function was intact in RIAM-deficient animals. These in vivo results confirm a role for RIAM in the regulation of some, but not all, leukocyte integrins and suggest that RIAM-regulated integrin activation is required for trafficking of lymphocytes from blood into pLNs and BM, where relatively high shear forces exist in high endothelial venules and sinusoids, respectively.

Published
2015
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249. Oxidative stress activates ADAM17/TACE and induces its target receptor shedding in platelets in a p38-dependent fashion.

Author

Brill, Alexander, Chauhan, Anil K., Canault, Matthias, Walsh, Meghan T., Bergmeier, Wolfgang, and Wagner, Denisa D.

Subjects
OXIDATIVE stress, BLOOD platelets, INFLAMMATION, OXIDATION-reduction reaction, PHYSIOLOGICAL stress
Abstract

Aims: Oxidative stress accompanies inflammatory and vascular diseases. The objective of this study was to explore whether reactive oxygen species can activate shedding of platelet receptors and thus suppress platelet function. [ABSTRACT FROM PUBLISHER]

Published
2009
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250. Regulated surface expression and shedding support a dual role for semaphorin 4D in platelet responses to vascular injury.

Author

Li Zhu, Bergmeier, Wolfgang, Jie Wu, Hong Jiang, Stalker, Timothy J., Cieslak, Marcin, Ran Fan, Boumsell, Laurence, Kumanogoh, Atsushi, Kikutani, Hitoshi, Tamagnone, Luca, Wagner, Denisa D., Milla, Marcos E., and Brass, Lawrence F.

Subjects
*MEMBRANE proteins, *BIOLOGICAL membranes, *PROTEINS, *NEOVASCULARIZATION, *MONOCYTES, *RETICULO-endothelial system
Abstract

Semaphorin 4D (sema4D; CD100) is an integral membrane protein and the ligand for two receptors, CD72 and plexin-B1. Soluble sema4D has been shown to evoke angiogenic responses from endothelial cells and impair monocyte migration, but the origin of soluble sema4D, particularly at sites of vascular injury, has been unclear. Here we show that platelets express sema4D and both of its receptors and provide evidence that these molecules promote thrombus formation. We also show that the surface expression of sema4D and CD72 increases during platelet activation, followed by the gradual shedding of the sema4D extracellular domain. Shedding is blocked by metalloprotease inhibitors and abolished in mouse platelets that lack the metalloprotease ADAM17 (TACE). Mice that lack sema4D exhibit delayed arterial occlusion after vascular injury in vivo, and their platelets show impaired collagen responses in vitro. In resting platelets, as in B lymphocytes, CD72 is associated with the protein tyrosine phosphatase SHP-1. Platelet activation causes dissociation of the complex, as does the addition of soluble sema4D. These findings suggest a dual role for sema4D in vascular responses to injury. As thrombus formation begins, platelet-associated sema4D can bind to its receptors on nearby platelets, promoting thrombus formation. As thrombus formation continues, sema4D is shed from the platelet surface and becomes available to interact with receptors on endothelial cells and monocytes, as well as continuing to interact with platelets. [ABSTRACT FROM AUTHOR]

Published
2007
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