scholarly journals Correction: Circulating Endothelial Cells in Refractory Pulmonary Hypertension in Children: Markers of Treatment Efficacy and Clinical Worsening

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
Author(s):  
Marilyne Levy ◽  
Damien Bonnet ◽  
Laetitia Mauge ◽  
David S. Celermajer ◽  
Pascale Gaussem ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Hypertension ◽  
Treatment Efficacy ◽  
Circulating Endothelial Cells ◽  
Hypertension In Children ◽  
Clinical Worsening

scholarly journals Circulating Endothelial Cells in Refractory Pulmonary Hypertension in Children: Markers of Treatment Efficacy and Clinical Worsening

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e65114 ◽  
Author(s):  
Marilyne Levy ◽  
Damien Bonnet ◽  
Laetitia Mauge ◽  
David S. Celermajer ◽  
Pascale Gaussem ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Hypertension ◽  
Treatment Efficacy ◽  
Circulating Endothelial Cells ◽  
Hypertension In Children ◽  
Clinical Worsening

scholarly journals Enhanced circulating levels of CD3 cells-derived extracellular vesicles in different forms of pulmonary hypertension

2019 ◽  
Vol 9 (3) ◽  
pp. 204589401986435 ◽  
Author(s):  
Djuro Kosanovic ◽  
Ujjwal Deo ◽  
Henning Gall ◽  
Balachandar Selvakumar ◽  
Susanne Herold ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Pulmonary Hypertension ◽  
Extracellular Vesicles ◽  
Inflammatory Cells ◽  
Circulating Endothelial Cells ◽  
Profound Knowledge ◽  
Life Threatening ◽  
Circulating Levels

It has been shown previously that increased circulating endothelial cells-derived extracellular vesicles represent an important pathological attribute of pulmonary hypertension. Although it is a well-known fact that inflammatory cells may also release extracellular vesicles, and pulmonary hypertension is a disease associated with abnormal inflammation, there is no profound knowledge with regard to the role of inflammatory cells-derived extracellular vesicles. Therefore, our study demonstrated that circulating levels of extracellular vesicles derived from T-cells are enhanced in various pulmonary hypertension forms and that endothelial cells-derived extracellular vesicles may have distinctive profiles in different clinical subgroups of pulmonary hypertension, which still remains as a poorly treatable and life-threatening disorder.

scholarly journals Distinct patterns of circulating endothelial cells in pulmonary hypertension

2010 ◽  
Vol 36 (6) ◽  
pp. 1284-1293 ◽  
Author(s):  
D. M. Smadja ◽  
L. Mauge ◽  
O. Sanchez ◽  
J.-S. Silvestre ◽  
C. Guerin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Hypertension ◽  
Circulating Endothelial Cells

scholarly journals Role of circulating endothelial cells in assessing the severity of systemic sclerosis and predicting its clinical worsening

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Maria Luisa Di Martino ◽  
Alessandra Frau ◽  
Francesca Losa ◽  
Emma Muggianu ◽  
Mario Nicola Mura ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Systemic Sclerosis ◽  
Activity Index ◽  
Pulmonary Involvement ◽  
Endothelial Damage ◽  
Circulating Endothelial Cells ◽  
Digital Ulcers ◽  
Small Vessels ◽  
Reliable Marker ◽  
Clinical Worsening

AbstractEndothelial damage and fibro-proliferative vasculopathy of small vessels are pathological hallmarks of systemic sclerosis (SSc). The consequence is the detachment of resident elements that become circulating endothelial cells (CECs). The aim of our study was to evaluate the potential of CECs as biomarker in SSc. We enrolled 50 patients with limited cutaneous (lcSSc) and diffuse cutaneous (dcSSc) subset of SSc, who underwent clinical evaluation to establish the organ involvement. CECs were measured by flow-cytometry utilizing a polychromatic panel. An evident difference was observed in CEC counts comparing controls to SSc patients (median 10.5 vs. 152 cells/ml, p < 0.0001) and for the first time, between the two subsets of disease (median lcSSc 132 vs. dcSSc 716 CEC/ml, p < 0.0001). A significant correlation was established between CECs and some SSc clinical parameters, such as digital ulcers, skin and pulmonary involvement, presence of Scl-70 antibodies, nailfold videocapillaroscopy patterns and EUSTAR activity index. After 12 months, CECs correlated with clinical worsening of patients, showing that a number higher than 414 CEC/ml is a strong negative prognostic factor (RR 5.70). Our results indicate that CECs are a direct indicator of systemic vascular damage. Therefore, they can be used as a reliable marker of disease severity.

Circulating endothelial cells in pulmonary hypertension

2003 ◽  
Vol 90 (10) ◽  
pp. 698-703 ◽  
Author(s):  
Heiko Golpon ◽  
Robert Hebbel ◽  
Anna Solovey ◽  
Carlyne Cool ◽  
Rubin Tuder ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Hypertension ◽  
Peripheral Blood ◽  
Cell Activation ◽  
High Pressures ◽  
Circulating Endothelial Cells ◽  
Pulmonary Vasculature ◽  
Endothelial Cell Activation ◽  
Pulmonary Endothelium ◽  
The Individual

SummaryThe pulmonary endothelium plays a significant role in the pathobiology of Primary Pulmonary Hypertension. A number of diseases, related by a history of vascular injury, are associated with increased numbers of circulating endothelial cells (CECs). We hypothesized that patients with pulmonary hypertension would also have an increased number of circulating endothelial cells due to the high pressures and increased shear stress present within the pulmonary vasculature. We isolated the CECs from 14 patients with pulmonary hypertension, (5 primary and 11 secondary) and compared them to the cells from 12 normal controls. There was a significant increase in the number of CECs in peripheral blood in patients with both PPH and secondary pulmonary hypertension (SPH) when compared to normal volunteers (33.1 +/- 1.9 {PPH} and 27.2 +/- 6.9 {SPH} vs. 3.5 +/- 1.3 {controls}, p < 0.001). The number of circulating endothelial cells in the patient’s peripheral blood correlated significantly with the systolic, diastolic and mean pulmonary artery pressures of the individual. Approximately 50% of the CECs from patients with pulmonary hypertension expressed CD36, a marker of microvascular origin and 25% expressed E-selectin, a marker of endothelial cell activation. Although the origin of the CECs in patients with PH requires further investigation, one possible source is the pulmonary vasculature, and in patients with plexogenic pulmonary hypertension, the plexiform lesions. CECs may provide a non-invasive mean of accessing cells important to the pathobiology of severe pulmonary hypertension.

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