Platelet Surface Activation Markers after DDAVP Infusion in Healthy Subjects

12 plant species traditionally used by the Mapuche people in Chile to treat wounds and inflammations have been evaluated for their direct blood platelet inhibition. Seven of the 12 tested plant species showed platelet inhibitory effect in sheep blood, and four of these were also able to inhibit the ADP- (5.0 μM) and collagen- (2.0 μg/mL) induced aggregations in human blood. These four species in respective extracts (in brackets) wereBlechnum chilense(MeOH),Luma apiculata(H2O),Amomyrtus luma(DCM : MeOH 1 : 1) andCestrum parqui(DCM : MeOH 1 : 1). The platelet aggregating inhibitory effects ofA. luma(DCM : MeOH 1 : 1), andL. apiculata(H2O) were substantial and confirmed by inhibition of platelet surface activation markers.

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Study of Surface Activation Markers on CD3 ‐ CD16 + NK Cells and Their Correlation with Clinical Manifestations in Children with Infectious Mononucleosis

Microbiology and Immunology ◽

10.1111/1348-0421.12925 ◽

2021 ◽

Author(s):

Wanding Ye ◽

Wan Zhang ◽

Shixiong Wu ◽

Mengquan Zhu ◽

Zhiwei Xu

Keyword(s):

Nk Cells ◽

Infectious Mononucleosis ◽

Clinical Manifestations ◽

Surface Activation ◽

Activation Markers

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The Importance of Platelet Glycoside Residues in the Haemostasis of Patients with Immune Thrombocytopaenia

Journal of Clinical Medicine ◽

10.3390/jcm10081661 ◽

2021 ◽

Vol 10 (8) ◽

pp. 1661

Author(s):

Andrés Ramírez-López ◽

María Teresa Álvarez Román ◽

Elena Monzón Manzano ◽

Paula Acuña ◽

Elena G. Arias-Salgado ◽

...

Keyword(s):

Platelet Count ◽

Sialic Acid ◽

Healthy Controls ◽

Caspase Activity ◽

Antibody Dependent Cellular Cytotoxicity ◽

Activation Markers ◽

Platelet Surface ◽

Mannose Binding ◽

Transversal Study ◽

Binding Lectin

Loss of sialic acid from the carbohydrate side chains of platelet glycoproteins can affect platelet clearance, a proposed mechanism involved in the etiopathogenesis of immune thrombocytopaenia (ITP). We aimed to assess whether changes in platelet glycosylation in patients with ITP affected platelet counts, function, and apoptosis. This observational, prospective, and transversal study included 82 patients with chronic primary ITP and 115 healthy controls. We measured platelet activation markers and assayed platelet glycosylation and caspase activity, analysing samples using flow cytometry. Platelets from patients with ITP with a platelet count <30 × 103/µL presented less sialic acid. Levels of α1,6-fucose (a glycan residue that can directly regulate antibody-dependent cellular cytotoxicity) and α-mannose (which can be recognised by mannose-binding-lectin and activate the complement pathway) were increased in the platelets from these patients. Platelet surface exposure of other glycoside residues due to sialic acid loss inversely correlated with platelet count and the ability to be activated. Moreover, loss of sialic acid induced the ingestion of platelets by human hepatome HepG2 cells. Changes in glycoside composition of glycoproteins on the platelets’ surface impaired their functional capacity and increased their apoptosis. These changes in platelet glycoside residues appeared to be related to ITP severity.

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Vitamin D modulates the expression of HLA-DR and CD38 after in vitro activation of T-cells

Hormone Molecular Biology and Clinical Investigation ◽

10.1515/hmbci-2016-0037 ◽

2017 ◽

Vol 29 (3) ◽

Author(s):

Simon Villegas-Ospina ◽

Wbeimar Aguilar-Jimenez ◽

Sandra M. Gonzalez ◽

María T. Rugeles

Keyword(s):

Vitamin D ◽

Flow Cytometry ◽

Healthy Subjects ◽

Mononuclear Cells ◽

Activation Markers ◽

Hla Dr ◽

In Vitro Activation ◽

Cells Cultured

AbstractObjective:Vitamin D (VitD) is an anti-inflammatory hormone; however, some evidence shows that VitD may induce the expression of activation markers, such as CD38 and HLA-DR. We explored its effect on the expression of these markers on CD4Materials and methods:CD38 and HLA-DR expression was measured by flow cytometry in PHA/IL-2-activated mononuclear cells cultured under VitD precursors: three cholecalciferol (10Results:Cholecalciferol at 10Conclusion:Although no significant correlations were observed in vivo in healthy subjects, VitD treatment in vitro modulated immune activation by increasing the expression of CD38 and decreasing the proliferation of HLA-DR

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Abstract 113: Platelet and Monocyte Activity in Carotid Artery Stenosis Treated with Carotid Endarterectomy

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.36.suppl_1.113 ◽

2016 ◽

Vol 36 (suppl_1) ◽

Author(s):

Arvind Reddy Devanabanda ◽

Caron Rockman ◽

Nicole Allen ◽

Maya Rubin ◽

Binita Shah ◽

...

Keyword(s):

Carotid Artery ◽

Carotid Endarterectomy ◽

Carotid Artery Stenosis ◽

Healthy Subjects ◽

Artery Stenosis ◽

Monocyte Subsets ◽

Platelet Activity ◽

Platelet Surface ◽

Inflammatory Monocytes ◽

Anti Inflammatory

Background: Carotid artery stenosis (CAS) is a marker of atherosclerosis, a disease mediated by abnormalities in platelet and monocyte function, and a significant cause of stroke. Moreover, the effect of carotid artery revascularization via carotid endarterectomy (CEA) on platelet and monocyte markers is unknown. Objective: This study aims to investigate platelet activity, monocyte subsets and monocyte platelet aggregates (MPA) in CAS and changes with CEA. Methods: This prospective cohort study evaluated 48 patients who underwent non emergent CEA. Peripheral venous blood samples were obtained before, immediately postoperative and at 24 hours postoperative. Twenty healthy subjects served as controls. Platelet surface expression of P-selectin and PAC-1, monocyte subsets, and MPA were assessed using flow cytometry. Three distinct monocyte subsets were measured: anti-inflammatory (i.e. classical CD14 ++ CD16 - ) and pro-inflammatory (i.e. intermediate CD14 ++ CD16 + and nonclassical CD14 + CD16 ++ ) monocytes. Differences between two matched samples and between the study and control groups were statistically analyzed. Results: Compared to healthy subjects, CAS subjects had significantly greater markers of platelet activity (P-selectin [p=0.003] and PAC-1 [p=0.01]), pro-inflammatory monocytes (intermediate [p<0.0001] and nonclassical [p=0.009]) and MPA (p=0.0002). Following CEA, anti-inflammatory monocytes increased and pro-inflammatory monocytes decreased (Figure 1A). Platelet expression of P-selectin and MPA did not change, while PAC-1 transiently increased but then returned to baseline by 24 hours postoperative (Figure 1B &C). Conclusions: Subjects with CAS have elevated markers of thrombosis, inflammation, and their interface. However, only the pro-inflammatory monocytes are significantly reduced following CEA. Future studies investigating the clinical consequences of this reduction are warranted.

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Plasma Levels of Viro-Immunological Markers in HIV-Infected and Noninfected Ethiopians: Correlation with Cell Surface Activation Markers

Clinical Immunology ◽

10.1006/clim.2000.4958 ◽

2001 ◽

Vol 98 (2) ◽

pp. 212-219 ◽

Cited By ~ 19

Author(s):

Tsehaynesh Messele ◽

Margreet Brouwer ◽

Mulu Girma ◽

Arnaud L. Fontanet ◽

Frank Miedema ◽

...

Keyword(s):

Cell Surface ◽

Plasma Levels ◽

Surface Activation ◽

Activation Markers ◽

Immunological Markers

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Platelet Activation and Inhibition in Sickle Cell Disease (PAINS) Study

Blood ◽

10.1182/blood.v120.21.5147.5147 ◽

2012 ◽

Vol 120 (21) ◽

pp. 5147-5147

Author(s):

Andrew L. Frelinger ◽

Joseph A. Jakubowski ◽

Julie K. Brooks ◽

Sabrina L. Zayas ◽

Michelle A. Berny-Lang ◽

...

Keyword(s):

Sickle Cell Disease ◽

Antiplatelet Therapy ◽

Platelet Activation ◽

Healthy Subjects ◽

Research Funding ◽

Cell Disease ◽

Activation Markers ◽

Circulating Levels

Abstract Abstract 5147 Platelet activation/aggregation in sickle cell disease (SCD) may promote tissue ischemia, suggesting antiplatelet therapy may be useful. However, assessing platelet function and the effect of antiplatelet therapy in blood from SCD patients may be confounded by hemolysis with release of ADP. Here we evaluate levels of platelet activation markers in SCD adolescents vs. normal controls and compare, by multiple methods, the effect of in vitro blockade of the platelet ADP receptor P2Y12 by prasugrel's active metabolite, R-138727. Platelet activation markers in blood from SCD adolescents (n=15) and healthy adults (n=10), and the effect of R-138727 (0. 1 – 10 μM) added in vitro, were evaluated with and without ADP stimulation. Circulating levels of platelet-monocyte and platelet-neutrophil aggregates were significantly higher (p <0. 01) in SCD patients than in healthy controls. R-138727, in a concentration-dependent manner, inhibited platelet function in both SCD patients and healthy subjects as judged by ADP-stimulated light transmission aggregation, VerifyNow P2Y12 assay, multiple electrode aggregometry, and flow cytometric analysis of platelet vasodilator-stimulated phosphoprotein, activated GPIIb-IIIa and P-selectin. The R-138727 IC50s for each assay were not significantly different in SCD vs. healthy subjects. In summary: 1) The high circulating levels of platelet-monocyte and platelet-neutrophil aggregates demonstrate in vivo platelet activation in SCD and may be useful as markers of the in vivo pharmacodynamic efficacy of antiplatelet therapy in SCD. 2) The similar in vitro R-138727 IC50s in SCD and healthy subjects suggest that the prasugrel dose-dependence for platelet inhibition in SCD patients will be similar to that previously observed in healthy subjects. Disclosures: Frelinger: Eli Lilly: Consultancy, Research Funding; Daiichi Sankyo: Research Funding; GLSynthesis: Research Funding. Jakubowski:Eli Lilly: Employment. Heeney:Novartis: Consultancy, Research Funding; Eli Lilly and Company: Research Funding; Pfizer: Consultancy. Michelson:Eli Lilly: Data monitoring committee and idependent external monitor of clinical trials, Research Funding; Takeda: Research Funding; Oxygen Biotherapeutics: Research Funding; Alexion: Research Funding; Omthera: Research Funding.

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Concurrent and separate inside-out transition of platelet apoptosis and activation markers to the platelet surface

British Journal of Haematology ◽

10.1111/bjh.12529 ◽

2013 ◽

Vol 163 (3) ◽

pp. 377-384 ◽

Cited By ~ 12

Author(s):

Asuman Mutlu ◽

Armen V. Gyulkhandanyan ◽

John Freedman ◽

Valery Leytin

Keyword(s):

Activation Markers ◽

Platelet Surface ◽

Platelet Apoptosis ◽

Inside Out

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Cell Cycle Arrest during Measles Virus Infection: a G0-Like Block Leads to Suppression of Retinoblastoma Protein Expression

Journal of Virology ◽

10.1128/jvi.73.3.1894-1901.1999 ◽

1999 ◽

Vol 73 (3) ◽

pp. 1894-1901 ◽

Cited By ~ 63

Author(s):

Denise Naniche ◽

Steven I. Reed ◽

Michael B. A. Oldstone

Keyword(s):

Cell Cycle ◽

T Lymphocytes ◽

Measles Virus ◽

S Phase ◽

Surface Activation ◽

Quiescent State ◽

Activation Markers ◽

Infected Cells ◽

High Level ◽

Rna Levels

ABSTRACT One of the major mechanisms by which measles virus (MV) infection causes disease and death is suppression of the immune response. The nonresponsiveness of MV-infected human lymphocytes to mitogens and a partial block in the G0/G1 phase of the cell cycle observed in vitro is thought to reflect in vivo immunosuppression. In order to molecularly dissect MV-induced immunosuppression, we analyzed expression of surface activation markers and cell cycle-regulatory proteins in MV-infected human T lymphocytes. MV Edmonston (MV-Ed) could induce and maintain a high level of the early activation marker CD69 in the absence of proliferation. Expression of cyclins D3 and E, which positively control entry into S phase, was also significantly decreased. Analysis of inhibitors of progression into S phase showed that a high level of p27 was maintained in the G0/G1-blocked subpopulation of MV-Ed-infected cells compared to the proliferating MV-infected cells. Furthermore, cell cycle-related upregulation of retinoblastoma (Rb) protein synthesis did not occur in the MV-Ed-infected lymphocytes. Acridine orange staining, which distinguishes cells in G0from cells in G1, showed that RNA levels were not upregulated following activation, which is consistent with cells remaining in a G0 state. Although expression of surface activation markers indicated entry into the cycle, intracellular Rb and RNA levels suggested a quiescent state. These results indicate that MV can uncouple activation of T lymphocytes from transition of G0 to G1.

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