Microparticles in COVID-19 as a link between lung injury extension and thrombosis.

https://bit.ly/3eX2LPc.

Microparticles are new biomarkers of septic shock-induced disseminated intravascular coagulopathy.

Purpose: Septic shock-induced disseminated intravascular coagulopathy (DIC) contributes to multiple organ failure. Mechanisms governing vascular responses to open occurrence of DIC have not yet been established. Circulating plasma microparticles (MPs), released upon cell stress, constitute a catalytic procoagulant surface and are surrogates of vascular cell activation/injury.

Increased oxidative stress induces apoptosis in human cystic fibrosis cells.

Oxidative stress results in deleterious cell function in pathologies associated with inflammation. Here, we investigated the generation of superoxide anion as well as the anti-oxidant defense systems related to the isoforms of superoxide dismutases (SOD) in cystic fibrosis (CF) cells. Pro-apoptotic agents induced apoptosis in CF but not in control cells that was reduced by treatment with SOD mimetic.

Microparticles: a critical component in the nexus between inflammation, immunity, and thrombosis.

Plasma membrane remodeling characterized by phosphatidylserine exposure and consecutive microparticle (MP) shedding is an ubiquitous process enabling the clearance of senescent cells and the maintenance of tissue homeostasis. MPs are released as fragments from the budding plasma membrane of virtually all eukaryotic cell types undergoing stimulation or apoptosis and may be considered a broad primitive response to stress. MP release is dependent on cytoskeleton degradation pathways involving caspases, requires a sustained increase in intracellular calcium triggering K+ and Cl- efflux and is possibly tuned by mitochondria permeability changes.

Significance of membrane microparticles in solid graft and cellular transplantation.

Microparticles (MPs) are submicron vesicles released from stimulated or apoptotic cells after plasma membrane remodeling. In body fluids, they constitute relevant hallmarks of cell damage. Having long been considered inert debris reflecting cellular activation or damage, MPs are now considered as cellular effectors involved in cell-cell crosstalk.

A method to assess the migration properties of cell-derived microparticles within a living tissue.

Background: Cells undergoing activation or apoptosis exhibit plasma membrane changes, leading to the formation of shed vesicles (microparticles, MP). Although their effects on recipient cells in vitro, and their ability to support inflammatory or thrombotic events in the circulation have been studied, the spreading of such vesicles in tissues is still elusive. Our aim was to set up a method to examine the behavior of these vesicles in vivo.

Cellular mechanisms underlying the formation of circulating microparticles.

Microparticles (MPs) derived from platelets, monocytes, endothelial cells, red blood cells, and granulocytes may be detected in low concentrations in normal plasma and at increased levels in atherothrombotic cardiovascular diseases. The elucidation of the cellular mechanisms underlying the generation of circulating MPs is crucial for improving our understanding of their pathophysiological role in health and disease. The flopping of phosphatidylserine (PS) to the outer leaflet of the plasma membrane is the key event that will ultimately lead to the shedding of procoagulant MPs from activated or apoptotic cells.

Mechanisms of microparticle generation: on the trail of the mitochondrion!

Membrane remodeling, phosphatidylserine (PS) exposure, and subsequent microparticle (MP) shedding regulation is a critical step in maintaining vascular homeostasis. Shed MP, more particularly those of platelet origin, could be viewed as a way to increase the catalytic procoagulant surface relying on the essential presence of PS for optimal hemostatic response. Whether "flip-flop" is mandatory for the release of MP is suggested from the phenotype of Scott's syndrome, a rare bleeding disorder in which both PS exposure and MP shedding are deficient.

Circulating procoagulant microparticles in cancer patients.

Accumulating evidence indicates that microparticles (MPs) are important mediators of the interaction between cancer and the hemostatic system. We conducted a large prospective cohort study to determine whether the number of circulating procoagulant MPs is elevated in cancer patients and whether the elevated MP levels are predictive of occurrence of venous thrombembolism (VTE). We analyzed plasma samples of 728 cancer patients from the ongoing prospective observational Vienna Cancer and Thrombosis Study.

Factors influencing the level of circulating procoagulant microparticles in acute pulmonary embolism.

Background: Flow cytometry has shown levels of platelet-derived microparticles (PMPs) and endothelial-derived microparticles (EMPs) to be elevated in deep-vein thrombosis. Cardiovascular risk factors can also contribute to hypercoagulability due to circulating procoagulant microparticles (CPMPs).

Aims: To investigate in a case-control study the respective contribution of pulmonary embolism and cardiovascular risk factors to the level of hypercoagulability due to CPMPs.

Membrane microvesicles: macromessengers in cancer disease and progression.

Thrombotic complications have been documented in patients with cancer, and associated with tumor progression. Cancer patients have an increased level of circulating submicrometric (0.1-1 microm) membrane fragments termed microvesicles (MV) or microparticles.

Formation of procoagulant microparticles and properties.

The platelet procoagulant response consists of providing a catalytic surface where vitamin K-dependent clotting factors can interact with cofactors to form the characteristic enzyme complexes of the cascade culminating in the generation of sufficient thrombin for effective hemostasis. The essential element allowing such a local concentration is the anionic aminophospholipid phosphatidylserine, sequestered in the inner leaflet of the plasma membrane of resting cells but swiftly translocated to the outer leaflet after stimulation. Phosphatidylserine egress is followed by the shedding of membrane fragments, the so-called microparticles or microvesicles, also endowed with procoagulant properties more particularly when they harbor tissue factor, the major initiator of blood coagulation reactions.

Circulating procoagulant microparticles in acute pulmonary embolism: a case-control study.

We investigated whether circulating procoagulant microparticles (CPMPs) contributed to hypercoagulability in 45 patients with acute pulmonary embolism (APE) and in 45 controls with and 45 controls without cardiovascular risk factors. Concentrations of CPMPs and platelet-derived microparticles (PMPs) were statistically significantly higher in patients with APE than in controls without cardiovascular risk factors. PMPs appeared to be the main source of procoagulant microparticle release in APE, but this correlation disappeared when APE patients were compared to controls with cardiovascular risk factors.

Circulating microparticles may influence early carotid artery remodeling.

Objectives: To test associations of circulating microparticles with large artery remodeling before atherosclerosis is detectable.

Methods: In 232 untreated symptom-free individuals, we measured microparticles of various cellular origins (platelet, endothelial and leukocyte) by specific anti-GPIb (glycoprotein Ib), anti-cluster of differentiation (CD) 105 and anti-CD11a antibodies, and common carotid artery intima-media thickness (IMT), internal and external diameters by ultrasound.

Results: Except for CD105 microparticles with IMT to lumen ratio (IMT/D, P < 0.

Increased levels of circulating microparticles in primary Sjögren's syndrome, systemic lupus erythematosus and rheumatoid arthritis and relation with disease activity.

Introduction: Cell stimulation leads to the shedding of phosphatidylserine (PS)-rich microparticles (MPs). Because autoimmune diseases (AIDs) are characterized by cell activation, we investigated level of circulating MPs as a possible biomarker in primary Sjögren's syndrome (pSS), systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).

Methods: We measured plasma levels of total, platelet and leukocyte MPs by prothrombinase capture assay and flow cytometry in 43 patients with pSS, 20 with SLE and 24 with RA and in 44 healthy controls (HCs).

Translocator protein (18 kDa) is involved in primitive erythropoiesis in zebrafish.

The translocator protein (18 kDa) (TSPO), also known as peripheral-type benzodiazepine receptor, is directly or indirectly associated with many biological processes. Although extensively characterized, the specific function of TSPO during development remains unclear. It has been reported that TSPO is involved in a variety of mechanisms, including cell proliferation, apoptosis, regulation of mitochondrial functions, cholesterol transport and steroidogenesis, and porphyrin transport and heme synthesis.

Mechanisms of the noxious inflammatory cycle in cystic fibrosis.

Multiple evidences indicate that inflammation is an event occurring prior to infection in patients with cystic fibrosis. The self-perpetuating inflammatory cycle may play a pathogenic part in this disease. The role of the NF-kappaB pathway in enhanced production of inflammatory mediators is well documented.

Microparticles in endothelial cell and vascular homeostasis: are they really noxious?

Endothelial damage and release of membrane microparticles are key steps in the pathogenesis of inflammation. In this perspective article, Dr. Morel and co-workers discuss the biological and clinical significance of microparticles in endothelial cells.

Membrane microvesicles as actors in the establishment of a favorable prostatic tumoral niche: a role for activated fibroblasts and CX3CL1-CX3CR1 axis.

Tumor microenvironment is enriched in plasma membrane microvesicles (MV) shed from all cell types that constitute the tumor mass, reflecting the antigenic profile of the cells they originate from. Fibroblasts and tumor cells mutually communicate within tumor microenvironment. Recent evidences suggest that tumor-derived MVs (TMV) exert a broad array of biological functions in cell-to-cell communication.