Circulating Endothelial Cells in Patients with Venous Thromboembolism and Myeloproliferative Neoplasms

Abstract

BackgroundCirculating endothelial cells (CEC) may be a biomarker of vascular injury and pro-thrombotic tendency, while circulating endothelial progenitor cells (CEP) may be an indicator for angiogenesis and vascular remodelling. However, there is not a universally accepted standardized protocol to identify and quantify these cells and its clinical relevancy remains to be established.ObjectivesTo quantify CEC and CEP in patients with venous thromboembolism (VTE) and with myeloproliferative neoplasms (MPN), to characterize the CEC for the expression of activation (CD54, CD62E) and procoagulant (CD142) markers and to investigate whether they correlate with other clinical and laboratory data.Patients and MethodsSixteen patients with VTE, 17 patients with MPN and 20 healthy individuals were studied. The CEC and CEP were quantified and characterized in the blood using flow cytometry, and the demographic, clinical and laboratory data were obtained from hospital records.ResultsWe found the CEC counts were higher in both patient groups as compared to controls, whereas increased numbers of CEP were found only in patients with MPN. In addition, all disease groups had higher numbers of CD62E+ CEC as compared to controls, whereas only patients with VTE had increased numbers of CD142+ and CD54+ CEC. Moreover, the numbers of total and CD62+ CEC correlated positively with the white blood cells (WBC) counts in both groups of patients, while the numbers of CEP correlated positively with the WBC counts only in patients with MPN. In addition, in patients with VTE a positive correlation was found between the numbers of CD54+ CEC and the antithrombin levels, as well as between the CD142+ CEC counts and the number of thrombotic events.ConclusionsOur study suggests that CEC counts may reveal endothelial injury in patients with VTE and MPN and that CEC may express different activation-related phenotypes depending on the disease status.

Pulmonary Embolism and Splenic Infarction Caused by Polycythemia Vera

“…[6][7][8] Studies have found that the circulating endothelial cells in the blood of patients with PV are signi cantly higher than those in the normal control group, and their levels may also represent the degree of endothelial cell damages and disease progression. [8,9] Therefore, the vascular endothelial cells of patients with PV are damaged. Healthy endothelial cells can inhibit the activation of platelets, and when endothelial cells are damaged, it can promote the thrombosis.…”

La thrombose au cours des néoplasies myéloprolifératives

“…Il contribue à l'inhibition de l'adhérence des plaquettes et de l'activation de la coagulation. Au cours des néoplasies myéloprolifératives, plusieurs observations sont en faveur de l'existence d'une activation du compartiment endothélial : augmentation des taux circulants de thrombomoduline [27], de facteur von Willebrand (vWF) [27], de sélectines (E-et P-sélectine) [44], et de cellules endothéliales circulantes [45]. Acteur majeur de la vasorelaxation, l'oxyde nitrique (NO) est produit en moindre quantité par les cellules endothéliales de patients présentant une thrombocytémie essentielle [46].…”

Expression of CD markers in JAK2V617F positive myeloproliferative neoplasms: Prognostic significance

“… 72 , 73 CD142 (tissue factor), CD62P (P-selectin), and CD62E (E-selectin) are among the most common CD markers expressed following the activation of endothelial cells, which mediate the adhesion of platelets to these cells. 74 Furthermore, the increased expressions of intercellular and vascular adhesion molecules (including CD54 and CD106) on these cells, which play a role in the leuko-endothelial adhesion, might contribute to the prognosis of thrombotic events in JAK2 V617F positive disorders ( Table 1 ). 52 , 74 …”

“… 74 Furthermore, the increased expressions of intercellular and vascular adhesion molecules (including CD54 and CD106) on these cells, which play a role in the leuko-endothelial adhesion, might contribute to the prognosis of thrombotic events in JAK2 V617F positive disorders ( Table 1 ). 52 , 74 …”