Circulating microparticles: a marker of procoagulant state in normal pregnancy and pregnancy complicated by preeclampsia or intrauterine growth restriction

Bretelle, Florence; Sabatier, Florence; Desprez, Dominique; Camoin, Luc; Grunebaum, Lélia; Combes,; D’ercole, C.; Dignat-George, Françoise

doi:10.1055/s-0037-1613378

Cited by 136 publications

(100 citation statements)

References 28 publications

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“…Renal disease, [25][26][27] hypertension, 28 thrombotic thrombocytopenic purpura, 29 and pregnancy 30 promote the release of endothelial microparticles. A wide range of diseases and insults are also associated with the generation of platelet and leukocyte microparticles.…”

Section: Discussionmentioning

confidence: 99%

Cyclosporine Induces Endothelial Cell Release of Complement-Activating Microparticles

Renner¹,

Klawitter²,

Goldberg³

et al. 2013

Journal of the American Society of Nephrology

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Defective control of the alternative pathway of complement is an important risk factor for several renal diseases, including atypical hemolytic uremic syndrome. Infections, drugs, pregnancy, and hemodynamic insults can trigger episodes of atypical hemolytic uremic syndrome in susceptible patients. Although the mechanisms linking these clinical events with disease flares are unknown, recent work has revealed that each of these clinical conditions causes cells to release microparticles. We hypothesized that microparticles released from injured endothelial cells promote intrarenal complement activation. Calcineurin inhibitors cause vascular and renal injury and can trigger hemolytic uremic syndrome. Here, we show that endothelial cells exposed to cyclosporine in vitro and in vivo release microparticles that activate the alternative pathway of complement. Cyclosporine-induced microparticles caused injury to bystander endothelial cells and are associated with complement-mediated injury of the kidneys and vasculature in cyclosporine-treated mice. Cyclosporine-induced microparticles did not bind factor H, an alternative pathway regulatory protein present in plasma, explaining their complement-activating phenotype. Finally, we found that in renal transplant patients, the number of endothelial microparticles in plasma increases 2 weeks after starting tacrolimus, and treatment with tacrolimus associated with increased C3 deposition on endothelial microparticles in the plasma of some patients. These results suggest that injury-associated release of endothelial microparticles is an important mechanism by which systemic insults trigger intravascular complement activation and complement-dependent renal diseases.

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Section: Discussionmentioning

confidence: 99%

Cyclosporine Induces Endothelial Cell Release of Complement-Activating Microparticles

Renner¹,

Klawitter²,

Goldberg³

et al. 2013

Journal of the American Society of Nephrology

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“…Next, we assessed if the MP count elevated in vivo was also detectable in ACD tubes in pregnancy (a condition where elevated levels of PMPs and non-PMPs were reported previously in citrate tubes [23]). Indeed, there was a significant elevation in the PMP and non-PMP counts in pregnant women compared to non-pregnant healthy controls in citrate tubes (p = 0.002 and p = 0.004, respectively, Mann-Whitney Rank Sum test) (Fig.…”

Section: Detection Of Pregnancy Related Elevation Of Pmp and Non-pmp mentioning

confidence: 99%

Improved circulating microparticle analysis in acid-citrate dextrose (ACD) anticoagulant tube

György

Pálóczi

Kovacs

et al. 2014

Thrombosis Research

108

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Introduction: Recently extracellular vesicles (exosomes, microparticles also referred to as microvesicles and apoptotic bodies) have attracted substantial interest as potential biomarkers and therapeutic vehicles. However, analysis of microparticles in biological fluids is confounded by many factors such as the activation of cells in the blood collection tube that leads to in vitro vesiculation. In this study we aimed at identifying an anticoagulant that prevents in vitro vesiculation in blood plasma samples. Materials and Methods: We compared the levels of platelet microparticles and non-platelet-derived microparticles in platelet-free plasma samples of healthy donors. Platelet-free plasma samples were isolated using different anticoagulant tubes, and were analyzed by flow cytometry and Zymuphen assay. The extent of in vitro vesiculation was compared in citrate and acid-citrate-dextrose (ACD) tubes. Results: Agitation and storage of blood samples at 37°C for 1 hour induced a strong release of both platelet microparticles and non-platelet-derived microparticles. Strikingly, in vitro vesiculation related to blood sample handling and storage was prevented in samples in ACD tubes. Importantly, microparticle levels elevated in vivo remained detectable in ACD tubes. Conclusions: We propose the general use of the ACD tube instead of other conventional anticoagulant tubes for the assessment of plasma microparticles since it gives a more realistic picture of the in vivo levels of circulating microparticles and does not interfere with downstream protein or RNA analyses.© 2013 Elsevier Ltd. All rights reserved. IntroductionExtracellular vesicles (EVs) are membrane surrounded structures of various sizes (30-5000 nm) that have received significant attention recently [1]. EVs may be classified on the basis of their biogenesis, diameter and membrane markers. The two best characterized types of EVs include exosomes of endosomal origin and plasma membrane-derived microparticles (MPs) (recently often referred to also as microvesicles or ectosomes in the literature) [1]. EVs are present in all biological fluids including blood plasma, synovial fluid, cerebrospinal fluid, urine, tears and breast milk [1]. MPs are in between 100 and 1000 nm in diameter, and they are also detectable by flow cytometry [2,3]. Thus, MP profiles are easily analyzed in the routine clinical laboratory practice, and represent novel biomarkers of various diseases. In circulation, most MPs are derived from platelets, red blood cells, endothelial cells and leukocytes. Because of their abundance, platelet-derived MPs (PMPs) received the highest attention during the past few years. Elevated PMP counts are characteristic for nearly all autoimmune disorders [4,5], and also for several cardiovascular and metabolic diseases [1]. EVs not only contain proteins but also RNA molecules [1]. Extracellular RNA (exRNA) in blood plasma is encapsulated in EVs, or bound to either proteins or HDL molecules [6]. exRNAs, particularly miRNAs, are specific and sensitive biomarkers...

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“…P-Selectin rapidly shed from the cellular membrane of activated platelets [45] and P-selectin-exposing micro-particles with procoagulant activity were detected in the peripheral blood of women with PE [46,47]. However, there was no significant difference in P-selectin, catalase, and superoxide dismutase between PE (case group) and pregnant women with normal blood pressure (control group) in a recent study [48].…”

Section: P-selectinmentioning

confidence: 90%

Biomarkers and genetic factors for early prediction of pre-eclampsia

Kim

Shim

2017

J Genet Med

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JGMof the main causes of poor placental perfusion and leads to placental and fetal hypoxia. Hypoxia is a potent stimulus for release of the numerous factors into the maternal circulation that may affect endothelial function of maternal system, and this can be reason of hypertension and other signs of the disease.Currently, PE is thought to result from defective spiral artery remodeling, leading to cellular ischemia in the placenta and resulting widespread endothelial dysfunction of maternal multiorgan systems. Exact etiology underlying the cellular and molecular mechanisms of PE is still elusive. But recent observations support that altered expression of multiple factors is responsible for the clinical manifestation of the disease [4].PE is divided to 2 types; early-onset and late-onset PE. Earlyonset PE typically requires early delivery (before 34 weeks' gestation) as intrauterine growth retardation, unusual uterine and umbilical artery Doppler waveforms, and negative effects on the maternal and neonatal sides are common. Late-onset PE is commonly related to mild maternal disease and a low rate of

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Circulating microparticles: a marker of procoagulant state in normal pregnancy and pregnancy complicated by preeclampsia or intrauterine growth restriction

Cited by 136 publications

References 28 publications

Cyclosporine Induces Endothelial Cell Release of Complement-Activating Microparticles

Cyclosporine Induces Endothelial Cell Release of Complement-Activating Microparticles

Improved circulating microparticle analysis in acid-citrate dextrose (ACD) anticoagulant tube

Biomarkers and genetic factors for early prediction of pre-eclampsia

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