Thromb Haemost 2003; 90(04): 698-703
DOI: 10.1160/TH03-04-0251
Vascular Development and Vessel Remodelling
Schattauer GmbH

Circulating endothelial cells in pulmonary hypertension

Todd M. Bull
1   Division of Pulmonary Sciences and Critical Care Medicine, Pulmonary Hypertension Center, Denver Colorado, USA
,
Heiko Golpon
1   Division of Pulmonary Sciences and Critical Care Medicine, Pulmonary Hypertension Center, Denver Colorado, USA
,
Robert P. Hebbel
3   Vascular Biology Center and Division of Hematology-Oncology-Transplantation, University of Minnesota, Minneapolis Minnesota, USA
,
Anna Solovey
3   Vascular Biology Center and Division of Hematology-Oncology-Transplantation, University of Minnesota, Minneapolis Minnesota, USA
,
Carlyne D. Cool
2   Department of Pathology, University of Colorado Health Sciences Center, Denver Colorado, USA
,
Rubin M. Tuder
4   Department of Pathology, Johns Hopkins, Baltimore Maryland, USA
,
Mark W. Geraci
1   Division of Pulmonary Sciences and Critical Care Medicine, Pulmonary Hypertension Center, Denver Colorado, USA
,
Norbert F. Voelkel
1   Division of Pulmonary Sciences and Critical Care Medicine, Pulmonary Hypertension Center, Denver Colorado, USA
› Author Affiliations
Financial support: This research was supported through a grant from the Pulmonary Hypertension Association, administered through the American Heart Association and by a grant from the National Institute of Health (NIH), Grant Number 5POI HLGb254-02.
Further Information

Publication History

Received 28 April 2003

Accepted after revision 28 May 2003

Publication Date:
05 December 2017 (online)

Summary

The 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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