A novel flow cytometric approach to distinguish circulating endothelial cells from endothelial microparticles: Relevance for the evaluation of endothelial dysfunction

2012 ◽  
Vol 380 (1-2) ◽  
pp. 16-22 ◽  
Author(s):  
Paola Lanuti ◽  
Francesca Santilli ◽  
Marco Marchisio ◽  
Laura Pierdomenico ◽  
Ester Vitacolonna ◽  
...  
2011 ◽  
Vol 57 (12) ◽  
pp. 1757-1761 ◽  
Author(s):  
Sridevi Devaraj ◽  
Pappanaicken R Kumaresan ◽  
Ishwarlal Jialal

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.


2007 ◽  
Vol 25 (5) ◽  
pp. e1-e2 ◽  
Author(s):  
Françoise Dignat-George ◽  
Florence Sabatier ◽  
Andrew Blann ◽  
Alexander Woywodt

2007 ◽  
Vol 82 (8) ◽  
pp. 706-711 ◽  
Author(s):  
Hakan Ozdogu ◽  
Oktay Sozer ◽  
Can Boga ◽  
llknur Kozanoglu ◽  
Erkan Maytalman ◽  
...  

Author(s):  
Sergey A. Sayganov ◽  
Anastasiia M. Kuzmina-Krutetskaia

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.


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