scholarly journals Early Detection of Negative Smoking Impacts: Vascular Adaptation Deviation Based on Quantification of Circulated Endothelial Activation Markers

2021 ◽  
Vol Volume 17 ◽  
pp. 103-109
Author(s):  
Kumboyono Kumboyono ◽  
Wiwit Nurwidyaningtyas ◽  
Indah Nur Chomsy ◽  
Titin Andri Wihastuti
Keyword(s):  
Early Detection ◽  
Endothelial Activation ◽  
Activation Markers ◽  
Vascular Adaptation

scholarly journals Structural alterations and markers of endothelial activation in pulmonary and bronchial arteries in fatal asthma

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Renata Calciolari Rossi ◽  
Raquel Anonni ◽  
Diogenes Seraphim Ferreira ◽  
Luiz Fernando Ferraz da Silva ◽  
Thais Mauad
Keyword(s):  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Pulmonary Arteries ◽  
Endothelial Activation ◽  
Bronchial Arteries ◽  
Activation Markers ◽  
Asthma Attack ◽  
Collagen Iii ◽  
Asthma Patients ◽  
Fatal Asthma

Abstract Background There is interest in better understanding vessel pathology in asthma, given the findings of loss of peripheral vasculature associated with disease severity by imaging and altered markers of endothelial activation. To date, vascular changes in asthma have been described mainly at the submucosal capillary level of the bronchial microcirculation, with sparse information available on the pathology of bronchial and pulmonary arteries. The aim of this study was to describe structural and endothelial activation markers in bronchial arteries (BAs) and pulmonary arteries (PAs) of asthma patients who died during a fatal asthma attack. Methods Autopsy lung tissue was obtained from 21 smoking and non-smoking patients who died of an asthma attack and nine non-smoking control patients. Verhoeff–Masson trichrome staining was used to analyse the structure of arteries. Using immuno-histochemistry and image analyses, we quantified extracellular matrix (ECM) components (collagen I, collagen III, versican, tenascin, fibronectin, elastic fibres), adhesion molecules [vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1)] and markers of vascular tone/dysfunction [endothelin-1 (ET-1) and angiotensin II type 2 receptor (AT2)] in PAs and BAs. Results There were no significant differences in ECM components, ICAM-1, ET-1 or AT2 between asthma patients and controls. Smoking asthma patients presented with decreased content of collagen III in both BA (p = 0.046) and PA (p = 0.010) walls compared to non-smoking asthma patients. Asthma patients had increased VCAM-1 content in the BA wall (p = 0.026) but not in the PA wall. Conclusion Our data suggest that the mechanisms linking asthma and arterial functional abnormalities might involve systemic rather than local mediators. Loss of collagen III in the PA was observed in smoking asthma patients, and this was compatible with the degradative environment induced by cigarette smoking. Our data also reinforce the idea that the mechanisms of leukocyte efflux via adhesion molecules differ between bronchial and pulmonary circulation, which might be relevant to understanding and treating the distal lung in asthma.

Is the Efficacy of LDL Apheresis in Ischemic Optic Neuropathy Linked to a Reduction in Endothelial Activation Markers?

2006 ◽  
Vol 24 (4) ◽  
pp. 405-412 ◽  
Author(s):  
A. Ramunni ◽  
G. Ranieri ◽  
G. Giancipoli ◽  
S. Guerriero ◽  
R. Ria ◽  
...  
Keyword(s):  
Optic Neuropathy ◽  
Endothelial Activation ◽  
Ischemic Optic Neuropathy ◽  
Ldl Apheresis ◽  
Activation Markers

Carboxiterminal pro-endothelin-1 as an endothelial cell biomarker in thrombotic thrombocytopenic purpura

2016 ◽  
Vol 115 (05) ◽  
pp. 1034-1043 ◽  
Author(s):  
György Sinkovits ◽  
Péter Farkas ◽  
Dorottya Csuka ◽  
Katalin Rázsó ◽  
Marienn Réti ◽  
...  
Keyword(s):  
Thrombotic Thrombocytopenic Purpura ◽  
Acute Phase ◽  
Complement Activation ◽  
Endothelial Activation ◽  
Factor H ◽  
Healthy Controls ◽  
Activation Markers ◽  
Thrombocytopenic Purpura ◽  
Endothelin 1

SummaryThrombotic thrombocytopenic purpura (TTP) is characterised by the deficiency of the von Willebrand factor (VWF) cleaving protease (ADAMTS-13). Although several observations indicate an important role of endothelial activation in the pathogenesis of TTP, no reliable endothelial activation markers are available in the clinical management of TTP. Our aim was to investigate the presence of endothelial activation in TTP and to determine its connections with disease activity, therapy and complement activation. We enrolled 54 patients (median age 40.5; 44 females) and 57 healthy controls (median age 34; 30 females),VWF antigen, carboxiterminal-pro-endothelin-1 (CT-proET-1), complement Factor H and complement activation products (C3bBbP and SC5b-9) were measured. In both the acute and remission phase of TTP we found increased CT-proET-1 and VWF levels, while Factor H levels decreased compared with healthy controls. In remission, however, the elevated CT-proET-1 levels showed 22 % decrease when compared with the acute phase in paired samples (p=0.0031), whereas no changes for VWF and Factor H levels were observed. We also found positive correlations between CT-proET-1 levels and alternative pathway activation markers (C3bBbP; p=0.0360; r=0.4299). The data we present here demonstrate a role of endothelium activation in patients with acute TTP. The finding that CT-proET-1 levels decreased in remission compared with the acute phase further supports endothelial involvement. In addition, we show that endothelial activation also correlated with the activation of the alternative complement pathway. The data suggest that complement and endothelium activation jointly contribute to the development of TTP episodes in patients with predisposition to TTP.Supplementary Material to this article is available online at www.thrombosis-online.com.

scholarly journals Endothelial Activation Markers in Anemic Non-Dialysis Chronic Kidney Disease Patients

2008 ◽  
Vol 110 (4) ◽  
pp. c244-c250 ◽  
Author(s):  
Tejas V. Patel ◽  
Bharati V. Mittal ◽  
Sai Ram Keithi-Reddy ◽  
Jeremy S. Duffield ◽  
Ajay K. Singh
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Endothelial Activation ◽  
Activation Markers

Outcome assessment in the idiopathic inflammatory myopathies

2018 ◽  
Author(s):  
Lisa G. Rider ◽  
Frederick W. Miller
Keyword(s):  
Disease Activity ◽  
Endothelial Activation ◽  
Inactive Disease ◽  
Idiopathic Inflammatory Myopathies ◽  
Inflammatory Myopathies ◽  
Muscle Enzyme ◽  
Activation Markers ◽  
Core Set ◽  
Trial Endpoints ◽  
Muscle Ultrasound

Due to their rarity, heterogeneity, and multispecialty nature, the myositis syndromes have limited data-driven consensus on appropriate outcome measures. Recently, two international, multispecialty consortia developed new tools and consensus on core set measures of myositis disease activity and damage, as well as response criteria that are now recommended for use as clinical trial endpoints but will also be useful in clinical practice. Magnetic resonance imaging, muscle ultrasound, selected laboratory tests, and immunological biomarkers—including cytokines, chemokines, lymphocyte flow cytometry, and endothelial activation markers—can all be helpful adjuncts to serum muscle enzyme levels in assessing disease activity and damage, but these have not yet been fully validated. Definitions of clinically inactive disease, complete clinical response, and remission have also been proposed but require further validation. These advances should enhance the development of therapies by standardizing our ability to demonstrate their efficacy in treating the idiopathic inflammatory myopathies.

scholarly journals Endothelial Activation Markers and Their Key Regulators after Restrictive Bariatric Surgery*

Obesity ◽  
2007 ◽  
Vol 15 (6) ◽  
pp. 1395-1399 ◽  
Author(s):  
Jeroen Nijhuis ◽  
Francois M.H. van Dielen ◽  
Suomi M.G. Fouraschen ◽  
Maartje A.J. van den Broek ◽  
Sander S.M. Rensen ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Endothelial Activation ◽  
Activation Markers ◽  
Restrictive Bariatric Surgery

O217 The significance of endothelial activation markers in the prediction of subsequent development of preeclampsia

2009 ◽  
Vol 107 ◽  
pp. S155-S155
Author(s):  
M. Prochazka ◽  
I. Dhaifalah ◽  
J. Prochazkova ◽  
L. Slavik ◽  
J. Ulehlova ◽  
...  
Keyword(s):  
Subsequent Development ◽  
Endothelial Activation ◽  
Activation Markers

Antibodies Against Platelet Glycoprotein Target Antigens in Antiphospholipid Syndrome (APS).

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3973-3973 ◽  
Author(s):  
Carlos J. Bidot ◽  
Wenche Jy ◽  
Carlos Bidot ◽  
Lawrence L. Horstman ◽  
Vincenzo Fontana ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Antiphospholipid Syndrome ◽  
Antiphospholipid Antibodies ◽  
Dominant Role ◽  
Endothelial Activation ◽  
Platelet Glycoprotein ◽  
Activation Markers ◽  
Positive Group ◽  
Platelet Antibodies ◽  
Platelet Microparticles

Abstract Introduction: Antiphospholipid syndrome (APS) is characterized clinically by thrombotic events and the presence of antiphospholipid antibodies (aPLA) and/or lupus anticoagulant (LA). It is frequently associated with thrombocytopenia and anti-platelet antibodies have been implicated by some. However the roles of anti-platelet antibodies in APS have not been elucidated. We previously reported that platelet activation, but not endothelial activation, was associated with thrombosis in aPLA+ patients [Blood, 104:143a, 2004] but the cause of platelet activation was not addressed. In the present study, we investigated the prevalence of anti-platelet antibodies in APS patients, as well as platelet and endothelial activation. Material and Methods: We evaluated 47 patients with primary APS. Anti-platelet antibodies against GP IIb/IIIa (CD41b), GP Ib/IX (CD 42b) and GP IV (CD36) for IgG and IgM class were measured by PAICA assay [Thromb Haemost76:1820, 1996]. We also measured platelet and endothelial activation markers by flow cytometry: CD62P on platelets, CD31+/CD42+ platelet microparticles (PMP), and CD31+/CD42- endothelial microparticles (EMP). Results: Of the 47 patients, 34 (72%) were positive for at least one anti-platelet antibody. Looking first at IgG, 18/34 (53%) were positive for GP IV; 17/34 (50%) for GP IIb/IIIa; and 16/34 (47%) for GP Ib/IX. IgM antibodies were 47% (14/30) for GP Ib/IX, 38%(13/34) for GP IIb/IIIa, and 24% (8/33) for GP IV. Platelet and endothelial markers were significantly more common in the anti-platelet antibodies positive group: 40% vs. 21% for CD62P, 40% vs. 28.5% for EMP, and 23% vs. 5% for PMP, respectively. We found that CD62P associated significantly with IgM anti-GP IIb/IIIa (p< 0.05), and PMP with IgM anti-GP IIb/IIIa (p< 0.05), and IgM anti-GP IV (p< 0.05). Conclusions: Anti-platelet antibodies are common in APS, confirming previous reports. We found that anti-platelet antibodies IgM anti-GP IIb/IIIa, and IgM anti-GP IV were often associated with platelet activation, suggesting that these antibodies may activate platelets to play an important role in the thrombogenesis of APS. These antibodies were also associated with endothelial activation. It remains to be determined which antibodies, APLA and/or anti-platelet antibodies, play a dominant role in the activation of platelet or endothelial cells and contibute most to the pathogenesis of thrombosis in APS.

Hydroxyurea Therapy Reduces The Hypercoagulability State In a Sickle Cell Mouse Model

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 2234-2234
Author(s):  
Marina Pereira Colella ◽  
Camila Bononi Almeida ◽  
Nicola Conran ◽  
Flavia Rubia Pallis ◽  
Carla Fernanda Franco-Penteado ◽  
...  
Keyword(s):  
Sickle Cell ◽  
Plasma Levels ◽  
Bone Marrow Cells ◽  
Conflicts Of Interest ◽  
Endothelial Activation ◽  
Activation Markers ◽  
Thrombotic Complications ◽  
Hbf Induction ◽  
Elevated Rate ◽  
Cell Adhesion Molecule 1

Abstract Several lines of evidence show that sickle cell anemia (SCA) is characterized by a hypercoagulable state. SCA patients present an elevated rate of thrombotic complications and increased biological markers of coagulation activation. In a previous study we demonstrated that therapy with hydroxyurea (HU) in SCA patients was associated with reductions in hypercoagulability markers, in addition to reductions in hemolysis, inflammation and endothelial activation markers (Colella et al Journal of Thrombosis and Haemostasis 2012). In the present study, we attempted to further investigate whether the effect of HU on hemostatic activation is dependent on fetal haemoglobin (HbF) expression, hemolysis and/or inflammation. To do so, we used the BERK murine model of SCA, a homozygous model of SCA, incapable of expressing HbF. In this BERK model, treatment with HU results in no improvement in hemolysis, due to the lack of HbF induction (Lebensburger et al Haematologica 2010). The murine SCA model was generated by transplantation of nucleated bone marrow cells from BERK mice into lethally-irradiated C57BL6 mice. Only mice expressing > 97% of human hemoglobin S (HbS) at 10 weeks after transplantation were used in the study. HU therapy at the dose of 50mg/kg (HU group) or saline alone (control mice) was administered through intraperitoneal injections 5 times per week, initiated at 11 weeks after transplantation (approximate time of sickle marrow engraftment). After a treatment period of 16 weeks, blood samples drawn from the inferior cava vein were collected and submitted to evaluation of plasma levels of thrombin-antithrombin III (TAT), a final marker of thrombin generation, in both animal groups. We also evaluated plasma levels of the inflammation marker interleukin 6 (IL6), and the endothelial marker soluble vascular cell adhesion molecule-1 (sVCAM-1). TAT, IL6 and sVCAM-1 were all measured by commercially-available ELISA kits. Statistical analyses were performed using Mann-Whitney’s U test. Treatment with HU resulted in a significant reduction of TAT plasma levels (106.7 μg/L vs 138.5 μg/L; P = 0.05). Plasma levels of IL6 (7.1pg/mL vs 12.4pg/mL; P = 0.18) and sVCAM-1 (765.8 ng/mL vs 848.4 ng/mL; P= 0.43) presented non-significant reductions with HU treatment. Our results show that, in this murine SCA model, long-term HU treatment results in an improvement in the hypercoagulability state, even in the absence of HbF induction, or of a significant improvement of inflammation or endothelial activation. This indicates that HU may have a direct effect on inhibiting the activation of coagulation in SCA. Disclosures: No relevant conflicts of interest to declare.

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