Circulating endothelial cells: a new biomarker of endothelial dysfunction in hematological diseases

2016 ◽  
Vol 74 (4) ◽  
pp. 395-404 ◽  
Author(s):  
Nicolas Gendron ◽  
David M. Smadja
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Circulating Endothelial Cells ◽  
Hematological Diseases

scholarly journals Dynamics of endothelian function in different treatment strategies in stable ischemic heart disease

2019 ◽  
Vol 11 (1) ◽  
pp. 5-12
Author(s):  
Sergey A. Sayganov ◽  
Anastasiia M. Kuzmina-Krutetskaia
Keyword(s):  
Endothelial Cells ◽  
Heart Disease ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Ischemic Heart Disease ◽  
Peripheral Blood ◽  
Ischemic Heart ◽  
Circulating Endothelial Cells ◽  
Lipid Lowering ◽  
Stable Ischemic Heart Disease

Aim. To assess the dynamics of endothelial function by determining circulating endothelial cells in peripheral blood in patients with stable ischemic heart disease within various treatment approaches. Material and methods. The study involved 98 patients with stable ischemic heart disease and 30 patients in the control group without coronary atherosclerosis. Endothelial function was assessed by determining the number of circulating endothelial cells in peripheral blood using flow cytofluorimetry with antibodies to cell surface markers: CD146+CD45– at the baseline. Depending on the treatment tactics, the study participants were divided into 3 groups: the medicamental therapy group, the group of coronary stenting, and the group of coronary bypass surgery. After 3 months from the baseline, dinamics assessment of endothelial dysfunction was performed. Results. Endothelial dysfunction was observed in all patients with obstructive lesions of the coronary blood flow and associated with effort angina class and anatomical severity of coronary disease. Improvement of endothelial function was facilitated by lipid-lowering therapy. Revascularization by coronary stenting impaired endothelial function in three months after the intervention. Mycoardial revascularization by coronary bypass did not impair endothelial function. Conclusion. Examination of endothelial dysfunction by determining the number of circulating endothelial cells in peripheral blood can be used to assess the severity of endothelial dysfunction in patients with IHD receiving lipid-lowering therapy and undergoing surgical revascularization.

scholarly journals Convalescent COVID-19 patients are susceptible to endothelial dysfunction due to persistent immune activation

2020 ◽  
Author(s):  
Florence WJ Chioh ◽  
Siew-Wai Fong ◽  
Barnaby E. Young ◽  
Kan-Xing Wu ◽  
Anthony Siau ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cardiovascular Risk ◽  
Endothelial Dysfunction ◽  
Acute Infection ◽  
Vascular Complications ◽  
Preventive Therapy ◽  
Circulating Endothelial Cells ◽  
Vascular Events ◽  
Activation Markers ◽  
The Impact

ABSTRACTThe rapid rise of coronavirus disease 2019 patients who suffer from vascular events after their initial recovery is expected to lead to a worldwide shift in disease burden. We aim to investigate the impact of COVID-19 on the pathophysiological state of blood vessels in convalescent patients. Here, convalescent COVID-19 patients with or without preexisting conditions (i.e. hypertension, diabetes, hyperlipidemia) were compared to non-COVID-19 patients with matched cardiovascular risk factors or healthy participants. Convalescent patients had elevated circulating endothelial cells (CECs), and those with underlying cardiovascular risk had more pronounced endothelial activation hallmarks (ICAM1, P-selectin or CX3CL1) expressed by CECs. Multiplex microbead-based immunoassays revealed some levels of cytokine production sustained from acute infection to recovery phase. Several proinflammatory and activated T lymphocyte-associated cytokines correlated positively with CEC measures, implicating cytokine-driven endothelial dysfunction. Finally, the activation markers detected on CECs mapped to the counter receptors (i.e. ITGAL, SELPLG, and CX3CR1) found primarily on CD8+ T cells and natural killer cells, suggesting that activated endothelial cells could be targeted by cytotoxic effector cells. Clinical trials in preventive therapy for post-COVID-19 vascular complications may be needed.Graphical abstract

scholarly journals C-Reactive Protein Induces Release of Both Endothelial Microparticles and Circulating Endothelial Cells In Vitro and In Vivo: Further Evidence of Endothelial Dysfunction

2011 ◽  
Vol 57 (12) ◽  
pp. 1757-1761 ◽  
Author(s):  
Sridevi Devaraj ◽  
Pappanaicken R Kumaresan ◽  
Ishwarlal Jialal
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Oxidized Ldl ◽  
Circulating Endothelial Cells ◽  
Early Event ◽  
C Reactive Protein ◽  
Endothelial Microparticles ◽  
Reactive Protein

BACKGROUND Inflammation is pivotal in atherosclerosis. A key early event in atherosclerosis is endothelial dysfunction. C-reactive protein (CRP), the prototypic marker of inflammation in humans, is a risk marker for cardiovascular disease, and there is mounting evidence to support its role in atherothrombosis. CRP has been shown to promote endothelial dysfunction both in vitro and in vivo. Emerging biomarkers of endothelial dysfunction include circulating endothelial cells (CECs) and endothelial microparticles (EMPs). However, there is a paucity of data examining the effect of CRP on CEC and EMP production in vitro and in vivo. METHODS In this report, we treated human aortic endothelial cells (HAECs) with increasing concentrations of CRP (0–50 μg/mL) or boiled CRP. We counted CECs and EMPs by flow cytometry. RESULTS Although CRP treatment resulted in a significant increase in release of both CECs and EMPs, boiled CRP failed to have an effect. Pretreatment of HAECs with sepiapterin or diethylenetriamine NONOate, both of which preserve nitric oxide (NO), resulted in attenuation of CRP's effects on CECs and EMPs. CD32 and CD64 blocking antibodies but not CD16 antibody or lectin-like oxidized LDL receptor 1 small interfering RNA (LOX-1 siRNA) prevented CRP-induced production of CECs and EMPs. Furthermore, delivery of human CRP to Wistar rats compared with human serum albumin resulted in significantly increased CECs and EMPs, corroborating the in vitro findings. CONCLUSIONS We provide novel data that CRP, via NO deficiency, promotes endothelial dysfunction by inducing release of CECs and EMPs, which are biomarkers of endothelial dysfunction.

scholarly journals The role of adipocytokines and endothelial dysfunction with irritable bowel syndrome associated with obesity

2021 ◽  
Vol 11 (7) ◽  
pp. 219-227
Author(s):  
Yu. Bilooka ◽  
O. Fediv ◽  
H. Stupnytska ◽  
V. Bilookyi ◽  
O. Bilookyi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Irritable Bowel Syndrome ◽  
Endothelial Dysfunction ◽  
Blood Serum ◽  
Intercellular Adhesion ◽  
Circulating Endothelial Cells ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Endothelin 1 ◽  
Irritable Bowel

The article contains the analysis of results concerning investigation of adipocytokines content and endothelial dysfunction in 97 patients with irritable bowel syndrome associated with obesity. The blood serum was examined for the content of adipocytokines (leptin, adiponectin, resistin), stable nitrogen monoxide metabolites (nitrites/nitrates), endothelin-1, intercellular adhesion molecule 1 (ICAM-1), and the number of circulating endothelial cells (CEC).  Patients with IBS associated with obesity and prevailing diarrhea are found to develop a prominent imbalance of adipocytokines which is manifested in high levels of leptin and resisin and low level of adiponectin in the blood serum. Endothelial dysfunction evidenced by a high level of endothelin-1, the number of circulating endothelial cells, general NO and intercellular adhesion molecules 1, is characteristic for patients with IBS associated with obesity and prevailing diarrhea.

scholarly journals Sulodexide improves endothelial dysfunction in streptozotocin-induced diabetes in rats

2008 ◽  
pp. 491-494
Author(s):  
V Kristová ◽  
S Líšková ◽  
R Sotníková ◽  
R Vojtko ◽  
A Kurtanský
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Rat Aorta ◽  
Cardiovascular Complications ◽  
Mesenteric Arteries ◽  
Circulating Endothelial Cells ◽  
Protective Effects ◽  
Pharmacological Agents ◽  
Postprandial Plasma Glucose ◽  
Streptozotocin Induced Diabetes

Diabetes mellitus is associated with many complications including retinopathy, nephropathy, neuropathy and angiopathy. Increased cardiovascular risk is accompanied with diabetes-induced endothelial dysfunction. Pharmacological agents with endothelium-protective effects may decrease cardiovascular complications. In present study sulodexide (glycosaminoglycans composed from heparin-like and dermatan fractions) was chosen to evaluate its protective properties on endothelial dysfunction in diabetes. Effect of sulodexide treatment (SLX, 100 UI/kg/day, i.p.) in 5 and 10 weeks lasting streptozotocin-induced diabetes (30 mg/kg/day, i.p. administered for three consecutive days) was investigated. Animals were divided into four groups: control (injected with saline solution), control-treated with sulodexide (SLX), diabetic (DM) and diabetic-treated with sulodexide (DM+SLX). The pre-prandial and postprandial plasma glucose levels, number of circulating endothelial cells (EC) and acetylcholine-induced relaxation of isolated aorta and mesenteric artery were evaluated. Streptozotocin elicited hyperglycemia irrespective of SLX treatment. Streptozotocin-induced diabetes enhanced the number of circulating endothelial cells compared to controls. SLX treatment decreased the number of EC in 10-week diabetes. Acetylcholine-induced relaxation of mesenteric arteries was significantly impaired in 5 and 10-week diabetes. SLX administration improved relaxation to acetylcholine in 5 and 10- week diabetes. Diabetes impaired acetylcholine-induced relaxation of rat aorta irrespective of SLX treatment. Our results demonstrate that SLX treatment lowers the number of circulating endothelial cells and improves endothelium-dependent relaxation in small arteries. These findings suggest endothelium-protective effect of sulodexide in streptozotocin-induced diabetes.

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