Megakaryocyte-derived microvesicles, please stand up!

Ratajczak, Mariusz Z.

doi:10.1182/blood-2008-10-182964

Cited by 4 publications

(3 citation statements)

References 5 publications

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“…Interestingly, in healthy donors, the majority of circulating CD41+ PMPs do not express surface activation marker CD62P, suggesting that they do not originate from activated platelets. 62 In a very elegant study, Flaumenhaft et al report that a significant number of circulating CD41+ MPs in healthy individuals are derived directly from Mks. 63 Authors first demonstrated via electron microscopy of spontaneous formation of Mk-derived MPs (MkMPs) from cultured murine Mk and that these MkMPs were different from PMPs.…”

Section: How Do Megakaryocytes Target and Deliver Their Protein Cargomentioning

confidence: 99%

Megakaryocyte contribution to bone marrow fibrosis: many arrows in the quiver

Malara

Abbonante

Zingariello

et al. 2018

Mediterr J Hematol Infect Dis

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In Primary Myelofibrosis (PMF), megakaryocyte dysplasia/hyperplasia determines the release of inflammatory cytokines that, in turn, stimulate stromal cells and induce bone marrow fibrosis. The pathogenic mechanism and the cells responsible for progression to bone marrow fibrosis in PMF are not completely understood. This review article aims to provide an overview of the crucial role of megakaryocytes in myelofibrosis by discussing the role and the altered secretion of megakaryocyte-derived soluble factors, enzymes and extracellular matrices that are known to induce bone marrow fibrosis.

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Section: How Do Megakaryocytes Target and Deliver Their Protein Cargomentioning

confidence: 99%

Megakaryocyte contribution to bone marrow fibrosis: many arrows in the quiver

Malara

Abbonante

Zingariello

et al. 2018

Mediterr J Hematol Infect Dis

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“…Vehicle (saline) or LPS (500 ng/mL) was added to one of each paired aliquots of blood. At designated time points (5,30, and 60 minutes) after addition of vehicle or LPS, 10 mL whole blood from each aliquot was diluted into 990 mL (1:100) HEPES/ HANKS' buffer (130 mM NaCl, 5.4 mM KCl, 1.3 mM CaCl 2 , 0.8 mM MgSO 4 , 0.44 mM Na 2 HPO 4 , 20 mM HEPES, pH 7.4) with 1 mg/ml albumin and 1 mM STI for staining of platelets positive for leukocyte antigen and leukocyte positive for platelet antigen. The remaining blood was used to prepare platelet free plasma (PFP) for MV analysis.…”

Section: Experimental Design and Blood Collectionmentioning

confidence: 99%

“…These cell-derived vesicles are an interface of activation between cellular components of the blood with the vascular wall and between soluble components of the blood associated with immunity including response to infection [24,28,29]. For example, phosphatidylserine (PS) on the surface of MV provides catalytic sites for prothrombinase complex to generate thrombin needed for the conversion of fibrinogen to fibrin in formation of clots [25,30,31]. Furthermore, exposure of diluted blood to LPS in vitro increased production of platelet-derived as well as tissue factor positive MV within 3 to 6 hours [32,33,34].…”

Section: Introductionmentioning

confidence: 99%

Leukocyte- and Platelet-Derived Microvesicle Interactions following In Vitro and In Vivo Activation of Toll-Like Receptor 4 by Lipopolysaccharide

et al. 2011

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BackgroundPro-coagulant membrane microvesicles (MV) derived from platelets and leukocytes are shed into the circulation following receptor-mediated activation, cell-cell interaction, and apoptosis. Platelets are sentinel markers of toll-like receptor 4 (TLR4) activation. Experiments were designed to evaluate the time course and mechanism of direct interactions between platelets and leukocytes following acute activation of TLR4 by bacterial lipopolysaccharide (LPS).Methodology/Principal FindingsBlood from age-matched male and female wild type (WT) and TLR4 gene deleted (dTLR4) mice was incubated with ultra-pure E. coli LPS (500 ng/ml) for up to one hour. At designated periods, leukocyte antigen positive platelets, platelet antigen positive leukocytes and cell-derived MV were quantified by flow cytometry. Numbers of platelet- or leukocyte-derived MV did not increase within one hour following in vitro exposure of blood to LPS. However, with LPS stimulation numbers of platelets staining positive for both platelet- and leukocyte-specific antigens increased in blood derived from WT but not dTLR4 mice. This effect was blocked by inhibition of TLR4 signaling mediated by My88 and TRIF. Seven days after a single intravenous injection of LPS (500 ng/mouse or 20 ng/gm body wt) to WT mice, none of the platelets stained for leukocyte antigen. However, granulocytes, monocytes and apoptotic bodies stained positive for platelet antigens.Conclusions/SignificanceWithin one hour of exposure to LPS, leukocytes exchange surface antigens with platelets through TLR4 activation. In vivo, leukocyte expression of platelet antigen is retained after a single exposure to LPS following turn over of the platelet pool. Acute expression of leukocyte antigen on platelets within one hour of exposure to LPS and the sustained expression of platelet antigen on leukocytes following a single acute exposure to LPS in vivo explains, in part, associations of platelets and leukocytes in response to bacterial infection and changes in thrombotic propensity of the blood.

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RhoB/ROCK mediates oxygen–glucose deprivation-stimulated syncytiotrophoblast microparticle shedding in preeclampsia

Han

Yang

et al. 2016

Cell Tissue Res

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Increased circulating syncytiotrophoblast microparticles (STBMs) are often associated with preeclampsia (PE) but the molecular mechanisms regulating STBM shedding remain elusive. Experimental evidence has shown that actin plays a key role in STBM shedding and that Rho/ROCK is important in regulating actin rearrangement. To investigate the role of RhoB/ROCK-regulated actin arrangement in STBM shedding in PE, chorionic villous explants were prepared from placenta of patients with normotensive or PE pregnancies and BeWo cells were fused to imitate syncytiotrophoblasts. The oxygen-glucose deprivation (OGD) conditions were applied to imitate the pathophysiology of PE in vitro. The results showed that RhoB and ROCK were activated in the preeclamptic placenta, accompanied by increased actin polymerization and decreased outgrowing microvilli. In villous tissue cultures or BeWo cells, OGD activated RhoB, ROCK1 and ROCK2 and promoted STBM shedding and actin stress fibers formation. In BeWo cells, RhoB overexpression activated ROCK1 and ROCK2, leading to F-actin redistribution and STBM shedding and the OGD-induced actin polymerization and STBM shedding could be reversed by RhoB or ROCK knockdown. These results reveal that RhoB and ROCK play a key role in PE by targeting STBM shedding through actin rearrangement and that RhoB/ROCK intervention may be a potential therapeutic strategy for PE.

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Megakaryocyte-derived microvesicles, please stand up!

Cited by 4 publications

References 5 publications

Megakaryocyte contribution to bone marrow fibrosis: many arrows in the quiver

Megakaryocyte contribution to bone marrow fibrosis: many arrows in the quiver

Leukocyte- and Platelet-Derived Microvesicle Interactions following In Vitro and In Vivo Activation of Toll-Like Receptor 4 by Lipopolysaccharide

RhoB/ROCK mediates oxygen–glucose deprivation-stimulated syncytiotrophoblast microparticle shedding in preeclampsia

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