Circulating Progenitor and Mature Endothelial Cells in Deep Vein Thrombosis

Abstract

Introduction: Mature circulating endothelial cells (CEC) and circulating endothelial progenitor cells (EPC) have been described in several conditions associated with endothelial injury. Their role in deep vein thrombosis (DVT) has not been previously evaluated. Patients and Methods: In this pilot study we evaluated the time course of CEC and EPC release after vena cava experimental DVT in mice, using the FeCl3 model. We also evaluated their presence in patients with DVT at different phases of the disease (acute and chronic phase). CEC and EPC were evaluated by Flow Cytometry. Results: In mice, both CEC and EPC were increased 24 hours after DVT induction, peaking 48 hours thereafter. After 72 hours, CEC counts decreased sharply, whereas EPC counts decreased less substantially. In DVT patients we observed a significant increase in CEC counts immediately after DVT compared to healthy individuals. Patients with chronic disease also presented a significant elevation of these cell count. In a subgroup of patients for whom serial samples were available, CEC counts decreased significantly after 9-15 months of the acute event. Conclusions: Our results suggest the participation of these cells in the reparative processes that follows DVT, both at immediate and late time-points. The different kinetics of CEC and EPC release in experimental DVT suggests a heterogeneous role for these cells in the reparative events after DVT.

Circulating endothelial progenitor cells and endothelial cells in moyamoya disease

“…It has long been shown that the level of CECs is significantly higher in patients with widespread vascular damage, such as antineutrophil cytoplasmic antibody‐associated small vessel vasculitis (Woywodt, Streiber, et al., 2003), sickle cell crisis (Belcher et al., 2003), and pulmonary hypertension (Bull et al., 2003). Therefore, CECs have been used as a marker of endothelial damage in a variety of vascular disorders (Alessio et al., 2013; Davignon & Ganz, 2004; Dignat‐George & Sampol, 2000). Elevated CEC levels have been observed in various pathological conditions associated with vascular disease and are considered by some to be a biomarker of disease severity in vascular conditions (Erdbruegger, Haubitz, & Woywodt, 2006).…”

Endothelial Progenitor Cells influence acute and subacute stroke hemodynamics

“…No effect was identified by EPCs on early arterial recanalization. Although no previous study had assessed the association of EPCs with recanalization in ischemic stroke, early works on EPCs suggested the rationale for an effect on recanalization, albeit being more likely on venous thrombi, due to the organization of fibrin meshwork and cellular composition of the venous thrombi [21].…”

Endothelial progenitor cells accelerate the resolution of deep vein thrombosis

“…However, mature endothelial cells are terminally differentiated with a low proliferative potential [63]. Over the past decade, accumulating evidence indicates that a damaged endothelial lining can be restored by circulating EPCs [62,[64][65][66], which has challenged the traditional view of postnatal angiogenesis. Endogenous mobilization or injection of ex-vivo generated EPCs exhibit the capability of adhesion onto the injured vascular wall and accelerate endothelial regeneration [67].…”