Involvement of platelet glycoprotein Ib in platelet microparticle mediated neutrophil activation

Lo, Su Shun; Hung, Ching-Yu; Lin, Dong‐Tsamn; Peng, Hwei-Ling; Huang, Tur-Fu

doi:10.1007/s11373-006-9107-5

Cited by 47 publications

(31 citation statements)

References 48 publications

(45 reference statements)

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“…MPs are generated when cells undergo oxidative stress, apoptosis, or cell activation/calcium influx, and they are characterized by surface expression of antigenic markers from parent cells (8,9,14,25). As MPs bud from these cells, negatively charged phosphatidylserine residues are exposed, which often leads to secondary binding of annexin V. MPs can directly stimulate release of proinflammatory cytokines, and platelet-derived MPs stimulate leukocyte activation and aggregation (15,17,21). Annexin V-positive platelet-derived MPs exhibit procoagulant activity (2).…”

mentioning

confidence: 99%

Intramicroparticle nitrogen dioxide is a bubble nucleation site leading to decompression-induced neutrophil activation and vascular injury

Thom

Yang

Bhopale

et al. 2013

Journal of Applied Physiology

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Inert gases diffuse into tissues in proportion to ambient pressure, and when pressure is reduced, gas efflux forms bubbles due to the presence of gas cavitation nuclei that are predicted based on theory but have never been characterized. Decompression stress triggers elevations in number and diameter of circulating annexin V-coated microparticles (MPs) derived from vascular cells. Here we show that ∼10% MPs from wild-type (WT) but not inflammatory nitric oxide synthase-2 (iNOS) knockout (KO) mice increase in size when exposed to elevated air pressure ex vivo. This response is abrogated by a preceding exposure to hydrostatic pressure, demonstrating the presence of a preformed gas phase. These MPs have lower density than most particles, 10-fold enrichment in iNOS, and generate commensurately more reactive nitrogen species (RNS). Surprisingly, RNS only slowly diffuse from within MPs unless particles are subjected to osmotic stress or membrane cholesterol is removed. WT mice treated with iNOS inhibitor and KO mice exhibit less decompression-induced neutrophil activation and vascular leak. Contrary to injecting naïve mice with MPs from wild-type decompressed mice, injecting KO MPs triggers fewer proinflammatory events. We conclude that nitrogen dioxide is a nascent gas nucleation site synthesized in some MPs and is responsible for initiating postdecompression inflammatory injuries.

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mentioning

confidence: 99%

Intramicroparticle nitrogen dioxide is a bubble nucleation site leading to decompression-induced neutrophil activation and vascular injury

Thom

Yang

Bhopale

et al. 2013

Journal of Applied Physiology

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“…Similar to platelets, circulating PMPs can interact with PMNs via linkages including glycoprotein Ib/Mac-1, ␤ 2 -integrins (CD11b)/Mac-1, or P-selectin/PSGL-1 on PMPs/PMNs, thus causing PMN activation involving secretion of interleukin (IL)-8, oxidative burst, degranulation, and enhanced leukocyte rolling (79,99). Likewise, PMPs generated from LPS-stimulated platelets promote endothelial activation as exemplified by the finding that they further increase the IL-1␤-induced expression of vascular cell adhesion molecule-1 (30).…”

Section: Potential Detrimental Effects Of Microparticles In Alimentioning

confidence: 99%

“…Considerable research has focused on the direct interaction and communication between different cell types both in vivo and in vitro and has revealed important pathophysiological aspects of ALI. However, a rapidly growing number of studies have recently started to recognize the critical role of microparticles (MPs) as biomarkers, communication shuttles between these different cells and cell types, and independent functional effectors in a large variety of diseases ranging from endemic pathologies such as hypertension, diabetes, and atherosclerosis to frequently lethal syndromes such as ALI (7,16,27,28,31,36,44,60,65,79,99,118,129,135,138,155,172). Here we provide a brief overview on the main characteristics of MPs, review the current knowledge on their role in inflammatory disease with a particular focus on ALI, and oppose their proposed detrimental and beneficial effects in lung injury, thus providing a rationale for their future use as both therapeutic targets and tools.…”

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confidence: 99%

Microparticles and acute lung injury

McVey

Tabuchi

Kuebler

2012

American Journal of Physiology-Lung Cellular and Molecular Phys

125

118

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The pathophysiology of acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), is characterized by increased vascular and epithelial permeability, hypercoagulation and hypofibrinolysis, inflammation, and immune modulation. These detrimental changes are orchestrated by cross talk between a complex network of cells, mediators, and signaling pathways. A rapidly growing number of studies have reported the appearance of distinct populations of microparticles (MPs) in both the vascular and alveolar compartments in animal models of ALI/ARDS or respective patient populations, where they may serve as diagnostic and prognostic biomarkers. MPs are small cytosolic vesicles with an intact lipid bilayer that can be released by a variety of vascular, parenchymal, or blood cells and that contain membrane and cytosolic proteins, organelles, lipids, and RNA supplied from and characteristic for their respective parental cells. Owing to this endowment, MPs can effectively interact with other cell types via fusion, receptor-mediated interaction, uptake, or mediator release, thereby acting as intrinsic stimulators, modulators, or even attenuators in a variety of disease processes. This review summarizes current knowledge on the formation and potential functional role of different MPs in inflammatory diseases with a specific focus on ALI/ARDS. ALI has been associated with the formation of MPs from such diverse cellular origins as platelets, neutrophils, monocytes, lymphocytes, red blood cells, and endothelial and epithelial cells. Because of their considerable heterogeneity in terms of origin and functional properties, MPs may contribute via both harmful and beneficial effects to the characteristic pathological features of ALI/ARDS. A better understanding of the formation, function, and relevance of MPs may give rise to new promising therapeutic strategies to modulate coagulation, inflammation, endothelial function, and permeability either through removal or inhibition of “detrimental” MPs or through administration or stimulation of “favorable” MPs.

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“…Neutrophils are known to interact with circulating microparticles of nonleukocyte origin (28)(29)(30). Opportunities for neutrophilmicroparticle interaction are increased during SIRS, given a significant increase in circulating endothelial and platelet microparticles (28,31).…”

Section: Circulating Neutrophils During Systemic Inflammationmentioning

confidence: 99%

“…These complexes, although linked to improved patient outcomes, are also associated with augmented leukocyte activation (30). Indeed, platelet microparticles can activate neutrophils (29,32,33) and, in doing so, facilitate the progression of intravascular coagulation (34).…”

Section: Circulating Neutrophils During Systemic Inflammationmentioning

confidence: 99%

Neutrophil Intercellular Communication in Acute Lung Injury: Emerging Roles of Microparticles and Gap Junctions

Dengler

Downey

Tuder

et al. 2013

Am J Respir Cell Mol Biol

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A hallmark of acute inflammation involves the recruitment of polymorphonuclear leukocytes (neutrophils) to infected or injured tissues. The processes underlying this recruitment are complex, and include multiple mechanisms of intercellular communication between neutrophils and the inflamed tissue. In recent studies of the systemic and pulmonary vasculature, interest has increased in novel forms of intercellular communication, such as microparticle exchange and gap junctional intercellular communication. To understand the roles of these novel forms of communication in the onset, progression, and resolution of inflammatory lung injury (such as acute respiratory distress syndrome), we review the literature concerning the contributions of microparticle exchange and gap junctional intercellular communication to neutrophilalveolar crosstalk during pulmonary inflammation. By focusing on these cell-cell communications, we aim to demonstrate significant gaps of knowledge and identify areas of considerable need for further investigations of the processes of acute lung inflammation.Keywords: neutrophil; connexin; gap junction; microparticles; acute lung injury Although investigations of acute respiratory distress syndrome (ARDS) have yet to yield an efficacious pathophysiologytargeted therapy, they have provided important insights into the intercellular communications regulating neutrophil activation and alveolar transmigration. These communications include juxtacrine and paracrine (e.g., chemokines, cytokines, and proteinases), crosstalk between neutrophils and lung parenchymal cells, and the signaling conducted through cell-surface receptors such as leukocyte integrins and cognate adhesion molecules (e.g., intercellular adhesion molecules) expressed by lung parenchymal cells (1). The past decade has seen an increasing recognition of alternative forms of intercellular communications during the onset and resolution of inflammatory lung disease. These communications include microparticle exchange as well as gap junctional intercellular communication (GJIC). This Perspective will focus on these alternative forms of communication between neutrophils and lung parenchymal cells during the genesis of ARDS, highlighting opportunities for further investigations. MICROPARTICLE EXCHANGEMicroparticles are spherical, lipid bilayer-encapsulated extracellular bodies ranging from 50-1,000 nm in diameter. Microparticles can be secreted by almost every cell type, including lung parenchymal cells and inflammatory cells. Multiple forms of microparticles exist, reflecting different modes of production. "Exosomes" and "shedding vesicles" are derived from living cells, whereas "apoptotic bodies" are secreted by apoptotic and/or necrotic cells (2). Exosomes have an endosomal origin, and are stored as intraluminal vesicles within multivesicular bodies (3). Upon stimulation, exosomes are secreted by fusion with the cell membrane, forming a relatively homogenous group of microparticle sizes (50-150 nm). In contrast, shedding vesicles and apoptotic ...

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Involvement of platelet glycoprotein Ib in platelet microparticle mediated neutrophil activation

Cited by 47 publications

References 48 publications

Intramicroparticle nitrogen dioxide is a bubble nucleation site leading to decompression-induced neutrophil activation and vascular injury

Intramicroparticle nitrogen dioxide is a bubble nucleation site leading to decompression-induced neutrophil activation and vascular injury

Microparticles and acute lung injury

Neutrophil Intercellular Communication in Acute Lung Injury: Emerging Roles of Microparticles and Gap Junctions

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